1Why Ultrasound Physics Matters

Every sonographer needs physics knowledge for four core reasons:

1. Creating diagnostic images — understanding physics helps you produce clear, accurate pictures
2. Identifying artifacts — things that appear on screen that aren’t real structures; physics tells you why they happen
3. Equipment maintenance — you can recognize when something is wrong with the machine
4. Registry exams — the SPI tests this directly

2Key Historical Figures

3The Pulse-Echo Technique

This is the foundation of all ultrasound imaging.

Step-by-step process

1. The transducer sends a short sound pulse into the body
2. Sound travels through tissue at 1,540 m/s
3. It hits a boundary (like your carotid artery wall) and some bounces back
4. The echo returns to the transducer
5. The machine times how long the return took → calculates depth
6. That depth gets plotted as a bright dot on screen
7. Repeat thousands of times per second → real-time image

4Speed of Sound & the 13 µs Rule

The machine assumes ALL soft tissue conducts sound at this speed. It uses this to calculate depth. If the actual speed is very different (bone, air), the image distorts.

The 13-Microsecond Rule

• 1 microsecond = 0.000001 seconds
• Sound travels ~1 cm deep (round trip) in 13 µs
• 26 µs return = 2 cm deep
• 39 µs = 3 cm deep
• Pattern: depth in cm = return time ÷ 13

5Real-Time B-Mode Imaging

B-Mode = Brightness Mode. The standard 2D gray-scale image you see on every scan.

• Each returning echo = a bright dot on screen
• Stronger echo = brighter dot
• The transducer sweeps many narrow lines called scan lines across the tissue
• All those lines together = one complete frame
• ~30 frames per second = smooth, real-time video motion

6Scan Formats

7Doppler Ultrasound

Doppler detects and displays blood flow. It works on the Doppler Effect — the same reason an ambulance siren sounds higher-pitched as it approaches and lower as it leaves.

• Red blood cells moving toward the transducer → higher frequency echo
• Moving away → lower frequency echo
• Machine detects this frequency shift → displays as flow information

8Direct vs. Indirect Proportionality

• Direct proportion: When A goes up, B goes up. (More depth → more time for echo to return)
• Indirect / inverse proportion: When A goes up, B goes down. (Higher frequency → less penetration depth)

✨Cheat Sheet

⚠Common Beginner Mistakes

1. Forgetting 13 µs is round-trip — sound goes TO the structure AND comes back
2. Mixing up Curie and Doppler — Curie = crystals = transducer. Doppler = flow detection
3. Thinking B-Mode and Doppler are the same — B-mode shows anatomy; Doppler shows movement
4. Assuming all tissue is the same — the 1,540 m/s rule is an assumption; bone and air break it, causing artifacts

1The Receiver's Five Functions

After the transducer converts returning echoes to electrical signals, the receiver processes them — in order:

• 1. Amplification — boosts ALL signals equally (overall receiver gain)
• 2. Compensation — boosts deep echoes MORE to offset attenuation (TGC — making equal reflectors look equal regardless of depth)
• 3. Compression — squeezes the huge range of signal strengths into the range the display can show (dynamic range)
• 4. Demodulation — converts the electrical signal into a form suitable for display (rectify + smooth)
• 5. Rejection — discards low-level noise below a threshold

2The Scan Converter

• The scan converter translates the scan-line echo data into the image format the monitor displays — and stores it
• Analog storage (historic): signal stored as continuous voltages — prone to drift, fade, and degradation over time
• Digital storage (modern): signal stored as numbers — uniform, stable, instantly copyable, and it never degrades

3Pixels & Bits — the Digital Image

• Pixel density → spatial detail. More (smaller) pixels per image = finer detail resolved
• Bit depth → contrast. More bits per pixel = more shades of gray available = better contrast resolution

4Pre-Processing vs. Post-Processing

• Pre-processing = BEFORE the freeze — applied to data as it's acquired, during live scanning
• Post-processing = AFTER the freeze — applied to the stored image

5Automatic Image Processing

• Persistence — frame averaging: blends consecutive frames to smooth the image and suppress noise. The cost: reduced temporal resolution (moving structures smear)
• Fill-in interpolation — the machine calculates values for missed pixels/scan lines from their neighbors, filling gaps in the image

6PACS

Picture Archiving and Communication System — the digital image network:

• Instant access to archived studies from any workstation
• No degradation — digital copies are perfect forever
• Teleradiology — images read remotely, anywhere

7Display Modes & Focal Points

• M-mode — motion over time along one line: the tool for fetal heart motion and cardiac valve timing
• 3D imaging — adds surface detail, used in conjunction with 2D (not a replacement)
• Multiple focal points — better lateral resolution through the whole depth of view — but each focus needs its own pulse per line, so frame rate drops

8Temporal Resolution & the 77,000 Limit

• Temporal resolution = the ability to precisely position moving structures — determined by frame rate
• Sound's speed sets a hard budget: lines per second × imaging depth (cm) can't exceed about 77,000, because each centimeter of depth costs 13 µs of round-trip time. At 10 cm, that's at most about 7,700 lines per second
• Total lines per second = lines per frame × focal points × frame rate — spend the budget wisely: more lines or foci = fewer frames

9The Doppler Processors

• FFT (Fast Fourier Transform) — the processor behind spectral Doppler (PW and CW): full velocity detail, quantitative
• Autocorrelation — the fast processor behind color Doppler: compares packet pulses to estimate mean velocity quickly across thousands of pixels
• Variance mode — used specifically in echocardiography to distinguish laminar from turbulent flow (tagging turbulence in green)

10Cheat Sheet

• Receiver, in order: Amplify → Compensate → Compress → Demodulate → Reject
• Scan converter: scan lines → display; digital = stable, no degradation
• Pixels = detail · bits = gray shades
• Pre = before freeze · post = after · write mag = pre (new pixels) · read mag = post (bigger pixels)
• Persistence smooths, costs temporal resolution · interpolation fills missed lines
• PACS: instant, lossless, teleradiology
• M-mode = motion (fetal heart) · multi-focus = better lateral res, slower frames
• Temporal budget: lines/sec × depth (cm) ≤ ~77,000
• FFT = spectral · autocorrelation = color · variance mode = echo turbulence

1The Two Requirements for Flow

Blood does not move on its own. Two conditions must be met:

• A patent (open) vessel — an unobstructed path from point A to point B
• A pressure gradient — a pressure difference between the two ends. Blood flows from HIGH pressure to LOW pressure, and the bigger the difference, the greater the flow

2Resistance — What Fights the Flow

Three properties resist blood's movement:

• Viscosity — the thickness of the fluid; thicker blood (higher hematocrit) flows less easily
• Friction — blood rubbing against the vessel walls converts flow energy to heat
• Inertia — the resistance of blood to changes in its motion (starting, stopping, speeding up)

3Poiseuille's Equation — Predicting Volume Flow

Poiseuille's equation predicts the volume of blood flowing through a vessel per unit time. The pieces:

• Flow increases with a larger pressure gradient and a larger vessel radius
• Flow decreases with higher viscosity and a longer vessel

4Laminar vs. Turbulent Flow

• Laminar flow — NORMAL. Blood moves in smooth, parallel layers: fastest in the center of the vessel, slowest along the walls (friction). The velocity profile across the vessel is a smooth bullet-nose curve
• Turbulent flow — ABNORMAL. The orderly layers break down into chaotic swirls and eddies moving in many directions and speeds — classically downstream of a stenosis (narrowing), where blood exits the tight spot at high velocity

5Pulsatile vs. Steady Flow — Arteries vs. Veins

• Pulsatile flow — ARTERIES. The heart's contract-relax cycle drives flow in surges: accelerating with systole, easing with diastole. Arterial Doppler waveforms show this rhythmic beat-to-beat pattern
• Steady flow — VEINS. Far from the heart's push, venous flow is relatively constant — but it is not immune to influence: it varies with breathing (respiratory phasicity) and responds to body position

6Hydrostatic Pressure — Gravity Joins the Party

Hydrostatic pressure is the pressure created by the weight of the blood column itself, and it depends entirely on body position:

• Lying flat (supine): everything is level with the heart — hydrostatic pressure is essentially zero throughout
• Standing: gravity pulls the blood column down — pressure in the ankle veins rises dramatically (the full weight of the column from heart to ankle), while vessels above the heart see negative values

7Cheat Sheet

• Flow needs: patent vessel + pressure gradient (high → low)
• Resistance: viscosity, friction, inertia
• Poiseuille: flow ∝ radius⁴ — double the radius, 16× the flow
• Laminar = normal, layered, fastest at center · Turbulent = abnormal, chaotic, after a stenosis
• Pulsatile = arteries · Steady/phasic = veins (varies with respiration)
• Hydrostatic pressure: zero supine, highest at the ankles standing

1The Doppler Effect

The Doppler effect is a change in frequency caused by motion. In sonography, the moving reflectors are red blood cells:

• Blood moving TOWARD the transducer → echoes return at a HIGHER frequency than transmitted → positive Doppler shift
• Blood moving AWAY → echoes return at a LOWER frequency → negative Doppler shift
• Doppler shift = received frequency − transmitted frequency

2The Doppler Equation

The shift depends on five pieces — and the machine solves the equation backwards to report velocity:

• Doppler shift = (2 × v × f₀ × cos θ) ÷ c
• v — blood velocity (what we actually want)
• f₀ — transmitted (operating) frequency: higher frequency → bigger shift
• cos θ — cosine of the angle between the beam and the flow direction
• c — propagation speed (1540 m/s in soft tissue)
• 2 — because the sound makes a round trip: the moving cell receives a shifted wave, then re-emits it shifted again

3Angles — the Cosine Rules Everything

• cos 0° = 1 — beam parallel to flow gives the maximum Doppler shift
• cos 90° = 0 — beam perpendicular to flow gives NO shift at all: the machine sees nothing, or garbage
• The sonographer tells the machine the flow direction with the angle-correct cursor, aligned parallel to the vessel walls

4Continuous Wave Doppler

• Two elements: one transmits continuously, the other receives continuously — sound never stops
• Measures everything along the overlapping beam path — it cannot tell WHERE along the line a shift came from: range ambiguity (no depth resolution)
• The payoff: with no pulses there is no sampling limit — CW never aliases, so it measures the highest velocities accurately
• No grayscale image; often a dedicated pencil probe

5Pulsed Wave Doppler

• One element (or array) sends brief pulses, then listens — like imaging
• The sonographer places a sample volume (gate) at an exact depth — PW has range resolution: it knows exactly where the signal came from
• Placement rule: center of the vessel, where laminar flow is fastest and cleanest — not hugging the walls
• Duplex = grayscale image + PW Doppler displayed together: see the vessel, interrogate the flow
• The cost of pulsing: PW is limited by its sampling rate (PRF) — which brings us to aliasing

6Aliasing — the Wraparound Artifact

A pulsed system samples the flow intermittently. If the Doppler shift exceeds the Nyquist limit — PRF ÷ 2 — the machine can't keep up and the waveform wraps around: the peak gets cut off the top and pasted onto the bottom of the display, appearing as absurd reversed flow.

7Spectral Analysis — Reading the Waveform

• The machine runs the returning signal through spectral analysis (FFT), plotting velocity (vertical) against time (horizontal), with brightness showing how many cells travel at each velocity
• Normal laminar flow — cells move at similar speeds → a crisp waveform envelope with a clear, clean spectral window (the empty space under the trace)
• Turbulent flow — cells at many speeds and directions → the window fills in: spectral broadening, the signature of post-stenotic turbulence from the last lesson

8The Indices — PI & RI

Two calculations quantify how pulsatile or resistive a waveform is, using the velocities the spectrum already measured:

• Resistive Index (RI) = (peak systolic velocity − end diastolic velocity) ÷ peak systolic velocity
• Pulsatility Index (PI) = (maximum velocity − minimum velocity) ÷ mean velocity
• Higher values = higher downstream resistance. You've already used RI: the renal transplant threshold of 0.7–0.8 from abdominal sonography is this exact calculation

9Cheat Sheet

• Shift = received − transmitted · toward = positive · away = negative
• Equation: 2 v f₀ cos θ / c — the 2 is the round trip
• cos 90° = 0 → never 90° · angle correct ≤60°
• CW: 2 elements, continuous, range ambiguity, never aliases, highest velocities
• PW: pulses + gate, range resolution, duplex, aliases past Nyquist (PRF/2)
• Sample volume: center of the vessel
• Clean spectral window = laminar · spectral broadening = turbulence
• RI = (PSV−EDV)/PSV · PI = (Vmax−Vmin)/Vmean

1What Color Doppler Is

Color Doppler overlays flow information on the grayscale image — used in vascular imaging across every diagnostic ultrasound specialty. Under the hood it is pulsed-wave Doppler, so everything from the last lesson still applies (angles, Nyquist, aliasing).

• The machine sends multiple pulses per scan line — a group called a packet (ensemble) — and compares them to detect motion
• Color Doppler reports three things: flow direction, qualitative velocity (shade = speed class, not a number), and variance (how disorderly the flow is)
• Terminology: the PW sample volume is the “gate” — the color Doppler sample volume is the “color box”

2Packet Size — the Trade-Off Dial

3Color Maps — Reading the Bar

• The color bar on screen is the legend: the color on top of the baseline = flow TOWARD the transducer; the bottom color = flow AWAY (the classic BART default: Blue Away, Red Toward)
• On a velocity map, the shade carries speed: darker hues near the baseline = slow flow; brighter/lighter shades = faster flow
• Variance maps add a color (classically green) tagged onto turbulent, disorderly flow

4Color Aliasing — the Useful Artifact

• Color Doppler is pulsed, so it aliases past the Nyquist limit just like spectral PW — the color wraps through the brightest shades into the opposite color family (red→orange→yellow→light blue…)
• Tell it apart from true flow reversal: aliasing wraps through the LIGHT shades; real direction change passes through BLACK (through the baseline)

5Troubleshooting: the Black Vessel

A vessel sits inside the color box but shows no color. The class checklist:

• 90° angle — cos 90° = 0: steer the box or heel-toe the probe
• Disease — a blood clot (thrombus) or plaque filling the lumen: no flow to detect
• Color gain too low — turn it up until noise speckles, then back it off

6Power Doppler — the Sensitivity Specialist

Power Doppler maps the STRENGTH (amplitude) of the Doppler signal rather than the shift itself — essentially painting “there are moving cells here” in one color.

• Advantages: far more sensitive to slow and weak flow, and not angle-dependent — it works even near 90°, and it does not alias
• Disadvantages: NO direction information and NO velocity information — just presence of flow; also more sensitive to motion (flash artifact)
• When the class reaches for it: vertebral arteries, slow-flowing blood, and checking solid masses for vascularity

7Optimizing the Picture

• Steer the color box so the beam meets the vessel at a working angle — the optimal Doppler angle is 0° (maximum shift), so lean the box toward parallel
• Keep the box small — a huge box costs frame rate (more lines × packets per line)
• For spectral measurement, place the cursor in the vessel center and set the angle-correct parallel to the walls, ≤60°, as always

8Cheat Sheet

• Color Doppler = pulsed → angle-dependent, aliases at Nyquist
• Packet size ↑ = sensitivity ↑, frame rate ↓
• Color bar: top = toward · brighter shade = faster · red ≠ artery
• Aliasing wraps through light shades · true reversal passes through black
• Black vessel: 90°, clot/plaque, gain too low
• PW sample = gate · color sample = color box
• Power Doppler: amplitude only — most sensitive, angle-independent, no aliasing, no direction, no velocity

1What an Artifact Is — and Why They Happen

An artifact is anything in the image that doesn't represent real anatomy — something added, missing, misplaced, or mis-sized. They occur for three broad reasons:

• Physics violations — the machine builds the image on assumptions (sound travels in straight lines, at exactly 1540 m/s, echoes come only from the main beam, one trip out and back). When reality breaks an assumption — refraction bends the path, scattering redirects it, the beam picks up echoes from beyond where it's pointed — the image lies
• Equipment issues — malfunction or poor settings
• Improper operation — technique errors

2Resolution Artifacts

• Axial resolution artifact — two reflectors stacked along the beam, closer together than the system can separate, merge into one echo on screen
• Lateral resolution artifact — two reflectors side-by-side closer than the beam width merge into one; a tiny point reflector is also drawn as wide as the beam itself
• Section thickness (slice thickness) — the beam has a third dimension: thickness perpendicular to the imaging plane. Echoes from tissue just outside the plane get painted INTO it — the classic result: false debris inside a cyst, making a clean cyst look like it contains sludge or making a cyst mimic a solid mass
• Speckle — the grainy texture of parenchyma is not individual cells: it's the interference pattern of countless scattered echoes. It's a beneficial artifact — the tissue texture you diagnose with IS speckle

3Reverberation — the Bouncing Echo Family

• Reverberation — sound bounces back and forth between two strong parallel reflectors; each extra round trip arrives later, so the machine draws multiple equally-spaced lines marching deeper. Classic between the transducer and a strong shallow reflector
• Comet tail — a compact reverberation from a small, highly reflective object (surgical clip, crystal): a dense, tapering stripe of closely-spaced echoes. Old friend: the V-shaped comet tails of adenomyomatosis, from cholesterol crystals in the GB wall
• Ringdown — looks like a comet tail but the mechanism differs: fluid trapped between air bubbles resonates, sending a continuous stream of sound back — a long bright streak below gas. Associated with AIR, it can obscure the anatomy beneath and is difficult to eliminate

4Mirror Image, Multipath & Speed Error

• Mirror image — a strong specular reflector (the classic: the diaphragm) acts as a mirror: sound detours off it, hits a structure, and returns the long way. The machine, assuming a straight path, draws a duplicate of the structure on the FAR side of the reflector — always DEEPER than the real one (classic: “liver above the diaphragm”)
• Multipath — the echo's return trip takes an indirect route, so it arrives late and the reflector is drawn at the wrong, deeper position
• Speed error — the machine assumes 1540 m/s everywhere. When tissue is slower, echoes arrive late → the reflector is drawn TOO DEEP; faster tissue → drawn TOO SHALLOW. Boundaries can also step or displace where the beam crosses a different-speed region

5Cheat Sheet

• Artifact = on the image, not in the body — from physics violations, equipment, or operator
• Eliminate: plane · window · controls · position — real structures persist
• Axial/lateral res artifacts: too-close reflectors merge · section thickness: false debris in cysts · speckle: beneficial interference texture
• Reverb: equally-spaced repeats · comet tail: small metal/crystals (adenomyomatosis) · ringdown: AIR, hard to kill
• Mirror image: duplicate DEEPER, beyond the diaphragm · multipath: indirect return, drawn too deep · speed error: slow = too deep, fast = too shallow
• Part 2 covers the attenuation family (shadowing, enhancement) and the rest

1Why QA Exists — and Who Does What

• Quality assurance = regular testing and evaluation of the ultrasound system to guarantee the images it produces are diagnostically accurate — a drifting machine lies quietly
• Sonographers handle the daily care: inspection, cleaning, and reporting problems
• Service engineers and physicists run the formal performance evaluations — about every 4–6 weeks — using dedicated phantoms and test objects

2The Daily Care Routine

• Daily: inspect the machine and clean every touched component — keyboard, probes, cords
• Between every patient: clean the transducers — infection control is image control's sibling
• Weekly: a more thorough deep clean
• Always: keep detailed records of equipment issues and repairs — the paper trail is part of the QA program

3The AIUM Test Object

A rigid frame of precisely positioned pins (rods), arranged in groups — each pin group tests a specific performance metric:

• Dead zone — the shallow region near the transducer face the system cannot image; the shallowest pins reveal how deep it extends
• Axial resolution — a pin group with progressively tighter vertical spacing: the closest pair still shown separately marks the axial limit
• Lateral resolution — pins with tightening horizontal spacing do the same for the beam-width direction
• Depth (range) calibration — pins at known depths verify the machine places reflectors where they really are

4Tissue-Equivalent & Doppler Phantoms

• Tissue-equivalent phantom — built from material that mimics soft tissue (its attenuation and propagation speed), often with embedded “cysts” and “masses”: tests the machine under realistic conditions — sensitivity, gray scale, penetration, and overall image quality
• Doppler phantom — moving targets or flowing fluid that test the system's Doppler capabilities: flow detection and velocity accuracy

5Cheat Sheet

• QA = regular testing so the images stay trustworthy
• Engineers/physicists run phantoms every 4–6 weeks — sonographers don't use the tools
• Sonographer routine: daily inspect + clean touched parts · probes between patients · weekly deep clean · log everything
• AIUM test object: dead zone, axial & lateral resolution, depth calibration (pin groups)
• TE phantom: tissue-like — sensitivity, gray scale, penetration
• Doppler phantom: flow detection & velocity accuracy

1The Big Picture

• Ultrasound is non-ionizing — no radiation, and generally safe for patients
• No confirmed bioeffects have been documented from diagnostic ultrasound when intensities stay below the established limits
• The most real, documented injury risk in the room is ergonomic — to the sonographer: improper scanning posture and technique cause musculoskeletal injuries

2Dosimetric Quantities — Measuring the Dose

• Pressure — measured in pascals, using a hydrophone (a tiny transducer sampling the beam point by point)
• Power — total energy per time (watts)
• Intensity — power spread over area (W/cm²) — the quantity the safety limits are written in
• Beam intensity is characterized before machines ever reach the clinic, using the radiation force balance (total power) and hydrophone probes (point-by-point pressure)

3ALARA — the Operating Philosophy

• Never adjust the power (output) settings — use the presets: they exist so every exam starts at appropriate output. Need a better image? Reach for receiver gain, not output power

4Mode Intensities & Safe Levels

• Different modes deposit different intensities. Typical order, lowest to highest: B-mode (gray scale) → M-mode → color Doppler → PW spectral Doppler. Modes that keep the beam parked in one spot deliver the most energy to that spot
• The classic safe-intensity thresholds below which no bioeffects have ever been confirmed: unfocused beam < 100 mW/cm² · focused beam < 1 W/cm² (SPTA)

5MI, TI & Cavitation

• Thermal Index (TI) — the on-screen estimate of tissue heating risk: the higher the TI, the more heat the beam can deposit
• Mechanical Index (MI) — the on-screen estimate of mechanical (cavitation) risk from pressure swings
• Cavitation — the interaction of sound with microscopic gas bubbles in tissue:
  Stable cavitation — bubbles oscillate (swell and shrink) with the pressure wave without bursting
  Transient (inertial) cavitation — at higher pressures the bubbles collapse violently — the destructive form, capable of real tissue damage

6How Bioeffects Are Studied

• In vitro — “in glass”: cells and tissue samples in the lab
• In vivo — in living animals
• Epidemiological — human population studies comparing exposed and unexposed groups
• The verdict across all three: no harmful effects confirmed when intensities stay below the established limits

7Electrical, Mechanical & Ergonomic Safety

• Electrical: inspect cords and housings — cracked probe cases and frayed cables are shock hazards; report and pull damaged equipment
• Mechanical: the machine is heavy — lock the wheels, mind the cables, protect the probes
• Ergonomic (the real injury source): proper posture, arm support, and technique protect the sonographer's career — scanning injuries are the field's occupational hazard

8Cheat Sheet

• Non-ionizing · no confirmed bioeffects below limits · biggest real risk = sonographer ergonomics
• Pressure in pascals via hydrophone · total power via radiation force balance
• ALARA: indicated exams only · low intensity · minimal dwell · short-but-good exams
• Never touch output power — use presets; fix images with receiver gain
• Class: M-mode lowest, color Doppler highest intensity (book may say PW spectral — verify)
• No effects ever below: unfocused <100 mW/cm² · focused <1 W/cm²
• TI = heat · MI = cavitation · transient/inertial collapse = the dangerous cavitation
• Studies: in vitro · in vivo · epidemiological — all clear below limits

1The Liver at a Glance

The liver is the largest abdominal organ, living primarily in the right upper quadrant (RUQ). The left lobe typically crosses the midline into the LUQ — and in very thin or pediatric patients it can extend far enough to nearly touch the spleen.

• Normal adult length: 13–15 cm, measured at the right midclavicular line in the sagittal/longitudinal plane
• Smaller than normal = atrophic · Enlarged = hepatomegaly
• The liver moves inferiorly with inspiration

2Lobes of the Liver

Two systems divide the liver: lobar anatomy (what sonographers use) and Couinaud's segments (what surgeons use, based on hepatic and portal vein landmarks). These notes focus on lobar anatomy.

• Right lobe — the largest; shaped like an inverted pyramid; best imaged subcostally or transcostally
• Left lobe — pyramidal; sits anterior to the aorta; may reach the LUQ/spleen in thin or pediatric patients
• Caudate lobe — posterior-superior; directly anterior to the IVC; its sonographic landmark is the ligamentum venosum, a thin hyperechoic line directly anterior to it
• Quadrate lobe — no reliable sonographic landmarks; not clinically significant for scanning

3Coverings, Openings & Spaces

• Glisson's capsule — the smooth fibrous covering of the liver
• Bare area — the only part of the liver NOT covered by peritoneum
• Porta hepatis — the liver's “doorway”: portal vessels enter, bile ducts exit
• Morrison's pouch — the potential space between the liver and the right kidney

Keep the fluid vocab straight: ascites is free fluid in the peritoneal cavity (the abdomen). A pleural effusion is fluid around the lung in the chest — a different space, seen above the diaphragm.

4Dual Blood Supply

The liver is unique: it receives blood from two sources at once.

• Hepatic artery — branches from the celiac artery off the aorta; delivers fully oxygenated blood
• Portal vein — formed by the confluence of the superior mesenteric vein + splenic vein (with contribution from the inferior mesenteric vein); delivers semi-oxygenated, nutrient-rich blood from the gut for filtration

5Portal Veins vs. Hepatic Veins

Telling these apart on screen is a foundational skill. They break the “veins look alike” rule:

• Portal veins — walls appear hyperechoic (bright/white) from thicker walls and the surrounding fibro-fatty channel; run horizontally and intrasegmentally (within segments)
• Hepatic veins — true thin-walled draining veins; run longitudinally and intersegmentally (between segments); there are three (right, middle, left); they widen as they approach the IVC and drain into it

6The Portal Triad

Throughout the liver, three structures travel together as the portal triad:

• Hepatic artery — oxygenated blood IN
• Portal vein — blood for filtering IN
• Bile duct — bile OUT, toward the gallbladder for storage

7Transducer Orientation Refresher

Reading the screen correctly is half of abdominal scanning:

• Sagittal / longitudinal: top of screen = anterior, bottom = posterior, screen-left = superior (head), screen-right = inferior (feet)
• Transverse: top/bottom stay anterior/posterior, but the sides become patient right and patient left

Structures you may see while scanning the liver: diaphragm, right kidney, right adrenal gland, IVC, stomach, duodenum, pancreas, ascending and transverse colon, and the right colonic flexure.

1Segmental Anatomy — the Veins Draw the Map

The hepatic veins are the liver's dividing lines:

• Middle hepatic vein — divides the right lobe from the left lobe
• Right hepatic vein — divides the right lobe into anterior and posterior segments
• Left hepatic vein — divides the left lobe into medial and lateral segments

The main portal vein enters at the porta hepatis and branches into right and left portal veins. The right divides into anterior and posterior branches; the left divides into medial (ascending) and lateral branches. Portal veins run horizontally, intrasegmentally — within segments. Hepatic veins run intersegmentally — between them.

2Landmarks & Fissures

• Ligamentum venosum — thin hyperechoic line separating the left lobe from the caudate lobe
• Ligamentum teres — the obliterated umbilical vein; appears as a hyperechoic triangle in the left lobe in transverse plane
• Main lobar fissure — thin echogenic line running between the gallbladder and the right portal vein

3Liver Function Tests (LFTs)

Check the chart before you scan — the labs tell you what to look for:

• AST & ALT — the two primary LFTs; both elevated with liver cell necrosis (tissue death)
• Albumin — decreased when failing liver cells can no longer synthesize it
• Bilirubin — increased when the liver isn't processing it; causes jaundice (yellow-orange skin/eyes)
• AFP & CEA — tumor markers; may be elevated with primary or secondary liver cancer

4Normal Anatomic Variants

Variants look unusual but are not disease — the skill is recognizing them so you don't call pathology on normal anatomy:

• Riedel's lobe — a tongue-like extension of the right lobe, can reach the iliac crest, may be palpable, more common in females
• Caudate lobe size variation — fine as long as echogenicity and texture are normal
• Accessory hepatic veins — most people have three; some have two, some more
• Situs inversus — organs mirror-imaged to the opposite side; function is normal, orientation is disorienting

5Normal Appearance & the Grayscale Ladder

A normal liver is homogeneous — even texture, consistent gray — interrupted only by vessels, bile ducts, ligaments, and the occasional bowel gas. The diaphragm appears as a bright hyperechoic line above the liver from specular reflection (big, flat, smooth surface), not because it's hard tissue.

Darkest → brightest:

• Renal medulla (nearly anechoic) → renal cortex → liver → spleen → pancreas → renal sinus (brightest)
• The liver should be slightly brighter than renal cortex and slightly darker than pancreas and spleen

6Patient Prep & Positioning

• NPO 6–8 hours — minimizes bowel gas AND keeps the gallbladder distended with bile
• Positions: supine, LLD, RLD, oblique — annotate every position change
• Deep breath + hold does two jobs: pushes the diaphragm (and liver) inferiorly out from the ribs, and kills motion artifact

7Transducer & Machine Setup

• Curved linear, ~3–3.5 MHz for deep abdominal work; higher frequency for thin or pediatric patients
• Focus at or just below the area of interest
• Multiple focal zones: better lateral resolution, but the machine works harder — frame rate and temporal resolution drop. Use selectively.

8The Scanning Protocol

• Start sagittal at midline, sweep midline → patient's right through the whole liver
• Rotate to transverse, again midline → right, scanning superior → inferior
• Approaches: subcostal (angle up under the rib margin) and intercostal (between ribs)

1Diffuse vs. Focal — the Framing

Diffuse pathology affects the entire organ — the whole liver looks different from normal, in echogenicity and often in size. Focal pathology is localized: a mass, a spot, a region. This unit is about the diffuse processes.

2Fatty Liver Infiltration

Excess lipids/triglycerides accumulating inside hepatocytes. It's acquired, reversible if caught early, and benign — and it's one of the most common findings in abdominal ultrasound. Elevated ALT/AST on labs is often what triggers the exam order.

• Top two causes: obesity and chronic ETOH (alcohol) abuse
• Less common: diabetes, hyperlipidemia, tuberculosis, cystic fibrosis, certain medications

Sonographic appearance

• Liver enlarged (hepatomegaly) or normal in size
• Increased echogenicity — brighter than normal; granular, “lumpy and bumpy” texture
• Paucity of hepatic vessels — portal and hepatic veins hard to see
• Poor penetration — fat attenuates the beam
• Liver-kidney disparity — unusually bright liver next to an unusually dark-looking right kidney

3Focal Fatty Infiltration vs. Focal Sparing

Two mirror-image subcategories that both mimic masses:

• Focal fatty infiltration — patches of fat (hyperechoic) inside an otherwise normal liver → looks like a bright mass
• Focal sparing — patches of normal tissue (hypoechoic by comparison) inside an otherwise fatty liver → looks like a dark mass. Most common location: medial left lobe, just anterior to the porta hepatis

4Hepatitis

Inflammation of the liver, caused by hepatitis viruses A through F, spread via blood, fecal matter, and bodily fluids. B and C carry the most serious consequences — liver failure, cirrhosis, cancer.

Acute hepatitis

• Sudden onset: jaundice, anorexia, nausea, fatigue, diffuse joint pain
• Liver normal or DECREASED echogenicity (darker), may be enlarged and tender
• “Starry sky” — on the darkened liver, portal vein walls pop brighter by contrast
• Gallbladder wall may be thickened

Chronic hepatitis

• Coarse texture — like static on a TV screen
• INCREASED echogenicity (brighter); portal walls now look relatively dimmer against the bright liver

5Cirrhosis

Diffuse, irreversible, progressive replacement of normal parenchyma with fibrosis and abnormal nodules. Among the leading causes of death in the US — 60–70% of cases from chronic alcohol abuse. The only cure is transplant, requiring at least one year of sobriety for candidacy.

• Cardiac cirrhosis — from prolonged right-sided heart failure
• Biliary cirrhosis — from long-term bile duct obstruction

Early vs. late

• Early: looks like diffuse fatty liver — hepatomegaly, increased echogenicity, poor penetration
• Late: coarse texture, atrophy (sometimes the whole liver fits in one image), possible caudate lobe enlargement, ascites, dilated portal vein >13 mm, splenomegaly >13 cm, varices, hepatofugal flow, recanalized umbilical vein. Labs: elevated AST, ALT, bilirubin → non-obstructive jaundice

6Portal Hypertension — the Domino Chain

A fibrotic liver is as dense as scar tissue. Portal blood can't get in, so pressure climbs from ~10 mmHg to 20–30+ mmHg. Then the dominoes fall backward through the system:

• Blood backs up → dilated portal vein (>13 mm), splenic vein, and SMV
• Splenic backup → splenomegaly (>13 cm)
• The body reroutes → portosystemic collaterals and varices (extra anechoic tubes with flow near liver, pancreas, gallbladder). Esophageal varices can rupture — life-threatening hemorrhage
• Old fetal plumbing reopens → recanalized umbilical vein
• Ascites accumulates

7Budd-Chiari Syndrome

Obstruction on the drainage side — the hepatic veins.

• Primary: segmental obstruction of the hepatic portion of the IVC
• Secondary: blood clots, hypercoagulability, pregnancy, birth control medications, hepatic/renal/adrenal tumors compressing the IVC, radiation therapy, leukemia, polycythemia vera
• Dilated hepatic veins can also come from congestive heart failure

1The Simple Cyst — Three Criteria, No Exceptions

A liver cyst is a fluid-filled, epithelial-lined mass — benign, usually asymptomatic, more common in females, favoring the right lobe, typically <3 cm.

Differentials for a cystic-looking liver lesion: degenerating metastatic tumor, echinococcal cyst, liver abscess, liver hematoma. That's why the criteria are strict.

2Echinococcal (Hydatid) Cyst

A parasitic infection — worm larvae from the feces of dogs, sheep, hogs, and cattle. Larvae hatch in the gut, penetrate the wall, and ride the portal vein to the liver in 50% of cases. Patients are typically jaundiced with elevated ALP (alkaline phosphatase). Always ask about travel history.

• Daughter cyst — a cyst within a cyst
• Water lily sign — the detached inner lining floating within the cyst
• Honeycomb appearance — complex internal architecture

3Liver Abscesses

Pyogenic abscess (bacterial)

• “Pyo” = pus. Most common bugs: E. coli, Clostridium, Bacteroides
• Routes in: biliary tree, portal vein, hepatic artery, direct extension
• Clinical: fever, pain, nausea/vomiting/diarrhea, leukocytosis, elevated LFTs, anemia (low red cells)
• Sono: right lobe most often; round/oval with poorly defined walls; mostly hypoechoic (can be anechoic or echogenic); posterior enhancement usually present — pus is fluid
• Great mimic: can look like necrotic tumor, hydatid cyst, hemorrhagic cyst, simple cyst

Amoebic abscess (parasitic)

• Amoebas from contaminated food or water → gut → portal vein → liver
• Their secretions can liquefy hepatic tissue — treat fast
• Sono: typically subcapsular; low-amplitude internal echoes (NOT fully anechoic); thick, irregular walls; good through transmission
• Clinical: fever, leukocytosis, elevated LFTs, pain, diarrhea, melena (black tarry stools); travel history is critical

4Benign Solid Neoplasms

Cavernous hemangioma — the most common benign liver tumor

• Vascular structure filled with blood; more common in females
• Classic home: posterior segment of the right lobe; usually <3 cm
• Classic look: round, highly echogenic (bright white), well-defined, no posterior enhancement
• Bigger ones get inhomogeneous — CT often characterizes further

Focal nodular hyperplasia (FNH)

• Rare, benign; females under 40; linked to long-term oral contraceptive use; usually incidental
• Normal hepatocytes arranged abnormally; can be hyper-, hypo-, or isoechoic
• No malignant potential — biopsy confirms, then monitor

Liver cell adenoma

• Like FNH but lacks bile duct elements and Kupffer cells
• Linked to OCP use, anabolic steroids in men, and type 1 glycogen storage disease
• Right lobe; often large at detection (8–15 cm)
• Malignant potential → surgically removed upon discovery

Liver hematoma

• Blood collection outside a vessel — most commonly from blunt trauma (car accidents, altercations)
• Appearance evolves: new blood = darker; older clotted blood = brighter; usually mixed echogenicity
• Can closely mimic an abscess — differentiate with trauma history and decreased hematocrit/hemoglobin (vs. the abscess's fever + high WBC)

5Malignant Neoplasms

Hepatocellular carcinoma (HCC / hepatoma)

• The most common PRIMARY liver cancer (originates in the liver)
• About 80% of HCCs arise in a cirrhotic liver; chronic hepatitis B and C also raise risk
• Labs: may be normal, LFTs may be up; >50% have elevated AFP
• Sono: no specific appearance — solitary or multiple; hypo/hyper/iso/complex; distorts parenchyma; invades portal and hepatic veins; ascites common

Liver metastases — the most common liver malignancy overall

• Primary sites: GI tract, breast, lung; in children, the adrenal gland (neuroblastoma)
• Labs: elevated CEA and AFP possible; clinical: jaundice, pain, hepatomegaly, weight loss
• Sono: usually multiple solid lesions; two named patterns — the bullseye/target sign (concentric rings) and the moth-eaten pattern (bites taken out of the liver)

1Gallbladder Anatomy

A musculomembranous sac living in the gallbladder fossa on the posterior-inferior surface of the liver. Its one job: store bile. (In real life, it's green.)

• Fundus — the blunt, blind end
• Body — the middle
• Neck (infundibulum) — the narrowest part, and the only fixed portion, attached at the main lobar fissure

The body and fundus wander with body habitus, breathing, and bile fill — the gallbladder inflates and deflates like a balloon. Normal size: 7–10 cm long × ~3 cm wide. Hydropic (enlarged) when the transverse measurement exceeds 5 cm.

2The Biliary Tree — Follow the Bile

Bile is made by hepatocytes, then flows downhill:

• Intrahepatic ducts → right + left hepatic ducts → converge into the common hepatic duct
• The cystic duct (from the GB neck) joins the common hepatic duct → common bile duct (CBD)
• CBD runs posterior to the first portion of the duodenum, enters the posterior head of the pancreas, joins the main pancreatic duct
• Together they empty at the ampulla of Vater (hepatopancreatic ampulla) through the duodenal papilla, gated by the sphincter of Oddi

3Physiology & Lab Values

Bile is a surfactant for fat digestion — bile salts, cholesterol, and bilirubin (a hemoglobin-breakdown byproduct; it colors stool, and in excess, skin — jaundice). The hormone cholecystokinin (CCK), released by the duodenum when fatty food arrives, tells the gallbladder to contract.

• Indirect bilirubin ↑ — pre-hepatic problem or hepatic cell damage (liver can't conjugate it)
• Direct bilirubin ↑ — mechanical obstruction to bile flow outside the liver, pushing bilirubin into the bloodstream
• Alkaline phosphatase (ALP) ↑ — biliary obstruction (post-hepatic); bile leaks from ducts into blood

4Normal Variants

• Phrygian cap — fold between the fundus and body (named for the ancient conical cap)
• Junctional fold / Hartmann's pouch — fold between the body and neck; the most frequent GB variant
• Agenesis — congenitally absent GB (rare)
• Duplication — two gallbladders (extremely rare)
• Septations — hyperechoic lines within the lumen (rare)

5The Numbers to Memorize

• Wall: ≤3 mm — measured at the anterior wall in transverse
• CBD: 1–4 mm normal — plus up to 1 mm per decade after age 60, and up to 10 mm post-cholecystectomy
• GB: 7–10 cm × ~3 cm; hydropic when transverse >5 cm
• NPO: 8–12 hours (minimum 6) — distends the GB with bile, minimizes gas

6Scanning the Gallbladder

A normal fasting GB: anechoic lumen, thin echogenic wall (≤3 mm), posterior acoustic enhancement — bile is a weak attenuator, so the cyst rules apply.

• Scan sagittal + transverse — expect to hold the probe obliquely to get true GB planes
• Two positions: supine AND left lateral decubitus — mobile pathology (stones) shifts with gravity; fixed masses don't
• Highest frequency possible; small footprint helps intercostal windows
• Focus at or just below the posterior border; reduce gain until the lumen is clean black
• Murphy's sign: transducer pressure over the GB during deep breath — pain = positive

Pitfalls

• The anterior turn of the left portal vein can impersonate the GB — check against the main lobar fissure
• Folds mimic stones/polyps; Heister valves throw fake shadows (reposition to prove it)
• GB not visualized in a truly NPO patient? Suspect gallbladder disease — confirm NPO (ask about coffee with cream), ask about cholecystectomy, reschedule if needed

1Cholelithiasis (Gallstones)

Stones in the gallbladder — one of the most common findings in all of diagnostic ultrasound. About 10% of the population develops them; peak incidence in the 6th–7th decades, more in females (though anyone can get them at any age).

• The Four F's: Female, Fat, Fertile, Forty-plus (+ Familial history and Flatulence as bonus F's)
• Other risks: pancreatitis, cirrhosis, certain anemias, obesity, pregnancy, diabetes, biliary infections
• ~80% are asymptomatic. When symptomatic: RUQ pain 15–20 minutes after eating (fatty meals, dairy — the “gallbladder attack”), nausea, vomiting
• Most common cause: abnormal bile composition; also bile stasis (hospitalized/immobile patients) and biliary infection
• Stones alone are NOT an indication for surgery — many people live with them symptom-free

2Marie's Syndrome & Sludge

Marie's Syndrome

A stone impacted in the cystic duct or gallbladder neck compresses the common hepatic duct — bile can't leave the liver, so it backs up and the intrahepatic ducts dilate. On screen: an excess of anechoic tubular structures throughout the liver. (Some textbooks and the registry call this Mirizzi syndrome — same condition.)

• Color Doppler sorts the tubes: dilated ducts stay silent, vessels fill with color
• The GB may enlarge from impaired outflow
• Don't mistake the Heister valves' fake shadow for the impacted stone — reposition to check

Gallbladder sludge

• Echogenic bile from stasis — cholesterol crystals + calcium bilirubinate; common in hospitalized, immobile, or fasting patients
• Moves, does NOT shadow, layers in the dependent portion; the lumen loses its clean anechoic look
• A precursor to stones; sludge and stones often coexist

3Acute Cholecystitis

“-itis” = inflammation/infection. The most common trigger: a stone blocking the cystic duct, setting up bacterial infection. Clinical: acute RUQ pain (may radiate to the shoulder), fever, chills, nausea/vomiting. Labs: leukocytosis, ↑serum bilirubin, ↑transaminases, ↑ALP.

Complications when it goes bad: empyema (pus-filled GB), emphysematous cholecystitis (gas-forming bacteria in the wall), gangrene, perforation, pericholecystic abscess, ascending cholangitis, liver abscess, septicemia.

4Chronic Cholecystitis

• More common in elderly patients; repeated infection episodes secondary to stones
• Intermittent symptoms: vague RUQ/epigastric pain, referral to the scapula, intolerance to fatty foods, on-and-off nausea
• Labs: ↑LFTs (ALT/AST), ↑ALP, ↑direct bilirubin
• Sono: contracted GB with stones, hyperechoic irregularly thickened wall, or a non-functioning GB that never contracts; sludge possible

5The Benign Wall Club

Hydrops (mucocele)

• Prolonged complete cystic duct obstruction — bile is resorbed and replaced by wall-secreted mucus
• No inflammation: wall stays thin and normal; patient typically asymptomatic
• Key finding: transverse diameter >5 cm — a big round overfilled balloon from any angle

Polyps

• Benign, single or multiple; echogenic, NO shadow, NO movement — attached to the wall
• Measure and follow for growth

Porcelain gallbladder

• Calcified GB wall — stagnant bile, chronic low-grade infection, or stone irritation; rare
• Associated with cholelithiasis in 95% of cases; hard to see on US (the calcified wall shadows everything) — CT sees it better

Adenomyomatosis

• Benign proliferation of wall tissue — focal or diffuse; asymptomatic
• Hallmark: comet tail artifact from tiny stones trapped in the Rokitansky-Aschoff sinuses

Cholesterolosis (strawberry gallbladder)

• Local disturbance of cholesterol metabolism in the wall; benign, asymptomatic
• Small non-shadowing projections into the lumen, polyp-like; “strawberry” for the spotty gross-pathology look

6Gallbladder Carcinoma

• Rare but highly aggressive; elderly patients (70s–80s), more in females
• Almost always concurrent with cholelithiasis — stones are found trapped in the mass, though stones don't cause the cancer
• Spreads rapidly to the liver and neighbors; usually silent until already metastasized
• Late symptoms: appetite loss, nausea, vomiting, constant belching, RUQ pain, jaundice if the biliary tree is involved

1Choledochal Cysts

Congenital cyst-like dilations of the common bile duct, classified into five types by location — from a single extrahepatic cyst (Type 1) through intrahepatic + extrahepatic fusiform dilations (Type 4). Type 5 is Caroli's disease.

• Type 1 is the most clinically relevant: a cyst-like dilation near the porta hepatis, possibly with dilation of the CHD, CBD, and intrahepatic ducts
• Discovered in childhood: failure to thrive, intermittent jaundice, occasionally a palpable RUQ mass
• Rare — mostly seen in pediatric facilities; surgical correction once identified

2Caroli's Disease

• Congenital segmental dilation of the INTRAHEPATIC bile ducts — the classic “string of beads” on ultrasound
• Associated with infantile polycystic kidney disease and hepatic fibrosis
• Bile stasis in the dilated segments raises the risk of stone formation (lithiasis) and infection (cholangitis)
• Appears as multiple cyst-like areas that communicate with the bile ducts

3Biliary Obstruction — Intrinsic vs. Extrinsic

Anything impeding bile flow through the ducts. Sort the causes by where they come from:

• Intrinsic (inside the ducts): choledocholithiasis, cholangiocarcinoma, cholangitis
• Extrinsic (outside the ducts): pancreatic mass (especially the head), pancreatitis, pancreatic pseudocyst, periductal adenopathy (enlarged nodes), hepatic mass

The dilation signs — learn the names

• Parallel channel / shotgun sign — the dilated duct matches the adjacent portal vein in size: a double-barrel shotgun
• Antler pattern — dilated right + left hepatic ducts and branches, like deer antlers
• Stellate branching — radiating dilated ducts with posterior enhancement
• “Too many tubes” — an excess of anechoic tubular structures in the liver
• Peripheral tubular lucencies — anechoic tubes out at the liver's edges

4Choledocholithiasis

Stones within the bile ducts — usually born in the gallbladder, migrating through the cystic duct into the CBD, and landing most often in the distal CBD near the ampulla of Vater.

• Risk profile: gallstone history, chronic cholecystitis, older age — and notably post-cholecystectomy patients, where stagnant bile can form stones directly in the ducts
• Presentation ranges from silent to jaundice, RUQ pain, fever, chills, hepatomegaly, ↑serum bilirubin
• On US: echogenic focus in the duct, often shadowing, with proximal ductal dilation

5Cholangiocarcinoma & Klatskin's Tumor

Malignant tumor of the bile ducts — elderly patients (typically >70), with elevated risk in ulcerative colitis; stones coexist in about one-third of cases.

• Scirrhous type — dilates the entire biliary tree (intra- + extrahepatic)
• Polypoid type — also dilates the entire tree
• Klatskin's tumor — sits at the bifurcation of the right and left hepatic ducts; dilates the INTRAHEPATIC ducts ONLY, and may show a non-union of the right and left hepatic ducts

Clinical: acute RUQ pain, biliary colic, jaundice, vague intestinal disturbances, weight loss, sometimes a palpable mass. Sono findings: ductal wall thickening >5 mm, soft-tissue masses in/around ducts, focal stricture or abrupt duct termination, and pronounced biliary dilation with a normal pancreas (which points the finger away from extrinsic pancreatic causes).

1Anatomy — Where and What

The pancreas is a retroperitoneal organ in the epigastric region — 10–15 cm long, wider than tall, described as tadpole, dumbbell, sausage, comma, or boomerang shaped. It is the only abdominal organ without a capsule, which is why it can't be palpated and why its borders blend into the neighborhood.

• Head — sits in the C-loop of the duodenum; the gastroduodenal artery (GDA) borders it anterolaterally, the distal CBD posterolaterally. The uncinate process is the hook off the head wrapping posterior to the SMV
• Neck — directly anterior to the SMV, between head and body; the portal-splenic confluence (SMV + splenic vein) forms the main portal vein here
• Body — the longest segment; anterior to the aorta, SMA, left renal vein, and splenic vein; rides slightly more anterior than the head over the spine
• Tail — the hardest to image; runs from the vertebral border to the splenic hilum; anterior to the left kidney, posterior to the stomach

2Two Jobs: Exocrine & Endocrine

Exocrine — digestion

• Acinar cells (in clusters called acini) secrete enzymes into the ducts, draining to the duodenum at the ampulla of Vater
• Lipase → fats · Trypsin → proteins · Amylase → carbohydrates
• CCK and gastrin stimulate the secretion

Endocrine — blood sugar (islets of Langerhans)

• Alpha cells → glucagon — raises blood sugar (stored in the liver, converted to glucose)
• Beta cells → insulin — lowers blood sugar (drives glucose into cells)
• Delta cells → somatostatin — auto-regulates the other two

3Lab Values

• Amylase — 2× or more = acute pancreatitis; also up in intestinal obstruction, mumps/salivary disease, acute cholecystitis, peptic ulcer perforation, renal failure; decreased in hepatitis/cirrhosis
• Lipase — up in acute pancreatitis or pancreatic cancer; stays elevated longer than amylase; also cholecystitis, cirrhosis, severe renal disease
• Serum glucose — elevated: diabetes mellitus, chronic liver disease; decreased: islet cell tumors

4Variants & Special Findings

• Annular pancreas — congenital; the head + uncinate wrap around the second portion of the duodenum like a ring, risking obstruction; more common in males; pain and recurrent vomiting; surgery if symptomatic
• Cystic fibrosis — autosomal recessive exocrine disease; mucus blocks the ducts, enzymes can't reach the gut; pancreas appears hyperechoic (fibro-fatty replacement), small, or heterogeneous
• Simple cysts — from ductal obstruction, or with adult polycystic kidney disease (cysts in kidneys, liver, spleen, and pancreas)

5Normal Appearance & the Ducts

• Homogeneous, smooth contour, slightly hyperechoic vs. the liver (isoechoic in children/young adults) — and it gets brighter with age from fat deposition
• Duct of Wirsung (main duct) — runs tail → head, joins the CBD at the ampulla of Vater; dilated if >2 mm in the body or >3 mm in the head
• Duct of Santorini (accessory) — in the head; not normally seen. Rule of thumb: if you can see a duct clearly, suspect dilation from obstruction

6Scanning the Invisible Organ

• NPO 8–12 hours, morning exams preferred; positions: supine, LLD, left oblique, semi-upright
• Low-frequency curved array (same as liver/GB); focus at or just below the posterior border
• Transverse + sagittal; evaluate head, neck, body, tail independently in each plane; check the peripancreatic region for adenopathy, fluid, vascular abnormalities

The visualization toolbox

• “Santa Claus” maneuver — push the belly out
• Deep breath and hold · Valsalva (brace like taking a punch — dilates the landmark vessels)
• Left lobe of the liver as an acoustic window
• Water through a straw — a fluid-filled stomach becomes a window onto the pancreas
• Elbows propped + deep breath to displace gas · color Doppler to light up the vessel map

1Acute Pancreatitis

A sudden inflammatory reaction: digestive juices leak from damaged ducts and start digesting the pancreas itself.

• Labs: amylase rises EARLIEST; lipase takes longer to result but stays elevated longer once treatment starts; WBC up; bilirubin up if biliary cause
• Clinical: severe epigastric pain, nausea, fever if infected, jaundice if the swollen pancreas compresses the bile duct
• Two forms: edematous (common) vs. necrotizing (serious — hemorrhage, higher morbidity/mortality)
• Complications: pseudocyst, phlegmon, hemorrhage, necrosis, abscess, duodenal obstruction — likelier with alcohol and recurrence
• Sono: enlarged, hypoechoic (fluid-engorged); focal hypoechoic areas can mimic tumors — check the labs (cancer and pancreatitis elevate different markers). CT is usually the definitive study

2Pseudocysts & Chronic Pancreatitis

Pancreatic pseudocyst — the most common complication

• Leaked pancreatic juices collect outside the pancreas; “pseudo” because it resembles a cyst but isn't a true epithelial-lined one
• Typically single, oval-to-round (molds to neighbors), smooth but THICKENED walls, anechoic to low-level echoes, posterior enhancement
• Most common home: the lesser sac — between the pancreatic tail and the splenic hilum. Also: anterior perirenal space, peritoneal cavity, mediastinum, LUQ near the spleen
• Often resolve on their own; drained if causing discomfort
• Phlegmon — an inflammatory mass of edema + enzyme leakage; may resolve or progress into a pseudocyst or abscess

Chronic pancreatitis

• Irreversible, progressive destruction, often from repeated acute episodes
• Sono: shrunken, lobulated, hyperechoic pancreas with possible calcifications and ductal dilation — the chronic rule (brighter + smaller) strikes again

3Cystadenomas & Islet Cell Tumors

• Cystadenoma — rare, typically benign cystic lesion; may show septations and thick walls. Its malignant counterpart, cystadenocarcinoma, is suggested when ascites or liver mets tag along

Islet cell tumors (body & tail territory)

• Classified functional vs. non-functional — non-functional carry higher malignancy risk
• Insulinoma — the most common; small, body/tail, usually benign; excess insulin → hypoglycemia, sweating, potential insulin shock
• Gastrinoma (G-cell tumor) — second most common; gastrin → excess stomach acid → Zollinger-Ellison syndrome (peptic ulcers in stomach, duodenum, upper small intestine); frequently malignant
• Glucagonoma — rare, high malignancy risk
• Benign vs. malignant cannot be told apart on ultrasound — biopsy required

4Pancreatic Adenocarcinoma

The most common pancreatic cancer — exocrine origin, very poor prognosis because early tumors are silent and detection usually comes after spread. ~80% arise in the HEAD.

• Risks: African American ethnicity, male sex, high-fat low-fruit/vegetable diet, smoking, direct family history, chronic pancreatitis, age >60
• Clinical: unexplained weight loss, appetite loss, chronic abdominal/back pain, PAINLESS jaundice, nausea/vomiting, black tarry stools
• Sono: hypoechoic mass with poorly defined borders, usually >2 cm at diagnosis; plus dilated biliary tree, liver mets, ascites, regional adenopathy, dilated pancreatic duct

5The Retroperitoneum

The space posterior to the peritoneal cavity — between the posterior parietal peritoneum and the posterior abdominal wall. Three subdivisions: anterior pararenal space, perirenal space, posterior pararenal space (mostly fat).

• Residents: kidneys, adrenal glands, ureters, portions of the pancreas (incl. the uncinate), duodenum, ascending + descending colon, aorta, IVC
• A “retroperitoneal ultrasound” order usually means: kidneys, bladder, ureters, and the great vessels

Retroperitoneal pathology

• Lymphadenopathy — oval hypoechoic masses; the node chain hugging the abdominal aorta is a common place to spot them; enlargement = infection or malignancy
• Tumors — lipoma (benign, fatty) vs. the malignant crowd: leiomyosarcoma, liposarcoma, histiocytoma — large heterogeneous masses; biopsy decides
• Fibrosis — scar tissue linked to Crohn's disease, methysergide, radiation, some infections; hypoechoic but homogeneous, well-defined masses
• Fluid collections — lymphoceles and urinomas; posterior enhancement, simple or septated, not cancerous

1Renal Anatomy — the Layout

Paired retroperitoneal organs flanking the spine between L1 and L3. The right kidney sits slightly LOWER than the left (the liver pushes it down) — and the left is ~0.5 cm longer. Both ride ~2.5 cm with respiration, sitting anterior to the psoas and quadratus lumborum muscles. The urinary tract: 2 kidneys, 2 ureters, 1 bladder, 1 urethra.

• Renal capsule — smooth true outer covering; Gerota's fascia wraps the kidney, perinephric fat, and adrenal gland together
• Cortex — outer parenchyma, ~1.5 cm thick; home to millions of nephrons, the functional units that make urine
• Medulla / pyramids — deep to the cortex; the most HYPOECHOIC structures in the abdomen; apices point toward the sinus and touch the minor calyces
• Columns of Burton — cortical tissue dipping between the pyramids
• Renal sinus — central fat-filled cavity: the most ECHOGENIC area of the abdomen
• Calyces → pelvis — minor and major calyces funnel urine into the renal pelvis (the expanded top of the ureter, a urine reservoir)
• Hilum — the medial doorway for the renal artery, vein, nerves, lymphatics, and ureter
• Trigone — the triangle on the bladder's posterior-inferior wall where the ureters enter and the urethra exits

2Vasculature & Physiology

• Renal veins are larger than the arteries — easier to see
• Right renal artery passes POSTERIOR to the IVC — and is the longer artery
• Left renal vein runs ANTERIOR to the aorta, POSTERIOR to the SMA — and is the longer vein
• Extra renal arteries off the aorta are a normal possibility

The kidney's jobs: dispose of metabolic waste (urine), maintain blood pressure via fluid volume, regulate acid/base, regulate serum electrolytes. Two hormones to know: aldosterone (sodium reabsorption, potassium secretion) and ADH (reduces water excreted).

3Renal Lab Values

• Serum creatinine — the most SPECIFIC renal value; normal 0.6–1.2 mg/dL; doesn't rise until ~50% of renal function is already lost
• BUN — less specific; normal 5–15 mg/dL; up with renal disease/damage/failure/obstruction — but also CHF, GI bleeds, shock, starvation; down with overhydration, pregnancy, liver failure, low protein intake
• Urinalysis adds uric acid, protein (proteinuria), pH, cells, casts — hydration extremes skew results

4The Variant Zoo

Number

• Bilateral renal agenesis — no kidneys; always fatal
• Unilateral agenesis — one missing; check for an ectopic location (pelvis) before calling it absent
• Supernumerary kidney — rare complete duplication; can be mistaken for a mass

Location

• Pelvic kidney · cross-fused ectopia (both on one side, fused) · thoracic kidney (diaphragmatic hernia in utero) · transplant (placed in the pelvis; the native kidney stays and atrophies)

Fusion & shape

• Horseshoe kidney — the most common fusion anomaly: lower poles fused, midline anterior to the aorta, usually above the umbilicus; risks recurrent infection, ureteral obstruction, trauma. Don't confuse the midline mass with an aortic aneurysm — tissue character and shape tell them apart
• Cake/lump kidney — medial surfaces fused in the pelvis, one ureter · Sigmoid kidney — S-shape, upper pole of one fused to lower pole of the other

Development

• Unilateral hypoplasia (small kidney, the other compensates) · persistent fetal lobulation (lobulated contour past age 5) · double collecting system (common — complete: two separate ureters into the bladder; incomplete: ureters unite first)
• Dromedary hump — a bulge on the LEFT kidney from splenic compression — a variant, not a mass
• Hypertrophied column of Burton — prominent cortical band between pyramids that mimics a mass but is normal

5Ultrasound Appearance & the Numbers

• Adult cortex: homogeneous, low-level echoes — hypoechoic to liver; smooth contour; transverse view = C-shape / Pac-Man (orientation mirrors between sides — label carefully)
• Infants (≤~3 months): cortex iso- or MORE echogenic than liver/spleen, with big prominent pyramids — do not call them cysts
• Arcuate arteries — bright specular dots at the corticomedullary junction

6Scanning & Pitfalls

• NPO 8–12 hours; positions: supine, LLD, LPO, RLD, RPO, prone as needed; deep held inspiration drops the kidneys and clears bowel
• Right kidney — the easy one: liver as the acoustic window, subcostal or intercostal
• Left kidney — the challenge: spleen window when possible, deep breath almost always required, intercostal preferred
• Transducer: 3–4 MHz standard; 5 MHz for thin patients or stone hunting; smaller footprint fights rib shadow; oblique the probe to the kidney's true axis

Pitfalls

• Failing to fully elongate the kidney → falsely short length
• Bowel gas hiding the poles · a prominent renal vein mimicking a cyst in the pelvis
• Dromedary hump / hypertrophied column of Burton read as masses
• A full bladder physiologically dilating the renal pelvis — not obstruction
• The gallbladder near the right lower pole mistaken for free fluid in Morrison's pouch
• Left/right orientation mislabeled in transverse

7The Adrenal (Suprarenal) Glands

• Two triangular endocrine glands on the anterosuperior aspect of each kidney, at T12; retroperitoneal, inside Gerota's fascia, embedded in fat
• Cortex — outer ~80% of the gland · Medulla — the center
• Hormones: catecholamines from the medulla (adrenaline/epinephrine, noradrenaline/norepinephrine), plus aldosterone (mineralocorticoid) and cortisol (glucocorticoid)

1Simple Renal Cysts

The same three criteria as everywhere else in the body — completely anechoic, well-defined walls, posterior acoustic enhancement. All three or it isn't simple. Extremely common: roughly half of patients over 50 have at least one.

• Arise in the cortex and expand outward from the surface
• Usually asymptomatic and found incidentally; large cysts can compress neighboring tissue → flank pain or even hypertension
• Management: typically just noted and followed; symptomatic ones can be aspirated under ultrasound guidance

2Cysts by Address

• Cortical cyst — in the cortex; the most common kind
• Parapelvic cyst — sits IN the renal sinus (lymphatic origin); the classic hydronephrosis mimic
• Peripelvic cysts — clustered around the pelvis region
• Perinephric cyst — under or on the capsule surface

3Polycystic Kidney Disease — Two Inheritances

ADPKD — autosomal DOMINANT (adult)

• Bilateral, enlarged kidneys with innumerable cysts of varying sizes — the normal architecture disappears
• Cysts also appear in the liver, spleen, and pancreas
• Clinical: hypertension, hematuria, flank pain, palpable masses; progressive renal failure typically in the 40s–50s → dialysis or transplant
• Dominant inheritance = 50% odds per child → family screening matters

ARPKD — autosomal RECESSIVE (infantile)

• Presents in infancy: bilateral, enlarged, ECHOGENIC kidneys
• The cysts are too tiny to resolve individually — countless microscopic interfaces reflect sound, so the kidneys look bright instead of cystic
• Poor prognosis; often fatal without intervention

4Multicystic Dysplastic Kidney (MCDK)

• Congenital and UNILATERAL — the bilateral form is incompatible with life
• The affected kidney is non-functioning: multiple non-communicating cysts of varying sizes — the classic “bunch of grapes” — with no identifiable renal pelvis and no normal parenchyma
• The healthy contralateral kidney undergoes compensatory hypertrophy
• Usually diagnosed in infancy (often prenatally)

5The Rest of the Cystic Family

Acquired cystic disease (the dialysis kidneys)

• Long-term dialysis patients develop cysts in their native kidneys — which are typically small and echogenic from end-stage disease
• These kidneys carry an increased risk of renal cell carcinoma — they get monitored, not ignored

Medullary sponge kidney

• Dilated collecting tubules within the pyramids → the pyramids turn ECHOGENIC (the reverse of their normally-darkest-in-the-abdomen look)
• Associated with nephrocalcinosis (calcium deposits in the medulla); usually asymptomatic and found incidentally

Medullary cystic disease

• Cysts at the corticomedullary junction; salt-wasting and renal failure in young adults — rare but serious

The syndromes

• von Hippel-Lindau — renal cysts plus a significantly increased renal cell carcinoma risk
• Tuberous sclerosis — renal cysts plus angiomyolipomas (benign fatty tumors, coming up with the solid masses)

1Renal Cell Carcinoma (RCC)

Also called hypernephroma or renal adenocarcinoma — the most common renal malignancy in adults (~85%). Males 2:1, typically ages 50–70. Risks: smoking, obesity, hypertension, long-term dialysis (acquired cystic disease), and von Hippel-Lindau — the last lesson's seeds sprouting.

• Classic clinical triad: hematuria (most common presenting sign) + flank pain + palpable mass — but the full triad appears in fewer than 10% and signals late disease
• Sono: solid mass of variable echogenicity that distorts the renal contour; may be iso-, hypo-, or hyperechoic
• Treatment: partial or radical nephrectomy

2The Benign Solid Masses

Angiomyolipoma (AML)

• Benign tumor of fat + muscle + blood vessels (the name spells it: angio-myo-lipoma)
• Classic look: markedly HYPERECHOIC, well-defined cortical mass — the fat makes it bright; more common in females
• Tuberous sclerosis association → multiple and bilateral AMLs
• Small ones: asymptomatic, followed. >4 cm: bleeding risk — spontaneous retroperitoneal hemorrhage

Oncocytoma

• Benign and rare; famous for the central stellate scar (spoke-wheel pattern)
• Imaging can't reliably distinguish it from RCC → these usually come out anyway

3The Rest of the Malignant Lineup

• Wilms tumor (nephroblastoma) — the most common renal malignancy in CHILDREN, typically ages 2–5; presents as a large palpable flank mass; like RCC it can invade the renal vein/IVC; good prognosis with treatment
• Transitional cell carcinoma (TCC) — arises from the urothelial lining of the collecting system (pelvis, ureters, bladder); presents with painless hematuria; sono: a hypoechoic mass inside the echogenic sinus; TCC is multifocal — one tumor means the entire urinary tract including the bladder gets checked
• Renal lymphoma — usually secondary involvement, often bilateral: hypoechoic masses or diffuse enlargement
• Metastases — from lung, breast, and other primaries

4Hydronephrosis — Grading & Causes

Dilation of the collecting system from obstructed urine flow. Graded by how far the dilation marches:

• Mild (Grade 1) — splaying of the renal pelvis only
• Moderate (Grade 2) — pelvis + calyces dilate — the “bear claw” look
• Severe (Grade 3) — massive dilation with cortical thinning — the parenchyma is being pressed to death

Causes by level

• Intrinsic (in the tract): stones, TCC, blood clots, sloughed papilla
• Extrinsic (pressing from outside): pregnancy (very common — usually right side), pelvic masses, retroperitoneal fibrosis, enlarged prostate (BPH)
• Bladder level & below: bladder tumor, urethral stricture, posterior urethral valves in male infants

False positives — don't call hydro on these

• Overdistended bladder physiologically dilating the pelvis → rescan post-void; true hydro persists
• Parapelvic cysts (no communication — the last lesson's test)
• Extrarenal pelvis — a normal pelvis ballooning outside the sinus
• Prominent renal vessels → color Doppler: vessels fill, urine doesn't
• Diuretics/overhydration mildly distending the system

5Renal Calculi (Stones)

Most common composition: calcium oxalate. The sono signature you already know: echogenic focus + posterior acoustic shadow — plus a renal bonus: the twinkle artifact on color Doppler, a rapidly alternating color mosaic behind the stone that helps confirm small ones.

• Three classic lodging sites: the UPJ (ureteropelvic junction), the pelvic brim (where the ureter crosses the iliac vessels), and the UVJ (ureterovesical junction) — the UVJ is the most common, the narrowest point
• Renal colic: severe flank pain radiating to the groin, hematuria, nausea/vomiting
• Stones ≤5 mm usually pass on their own; larger ones may need lithotripsy or intervention

1Pyelonephritis — Acute & Chronic

Acute pyelonephritis

• Kidney infection, usually ascending from the bladder — E. coli is the most common bug
• Clinical: fever, chills, flank pain, dysuria, pyuria (pus in urine)
• Ultrasound is often NORMAL in acute pyelonephritis — the diagnosis is clinical + labs. Imaging's job: rule out complications (abscess, obstruction)
• When visible: enlarged, hypoechoic kidney with loss of corticomedullary differentiation — the acute rule (darker + larger) holding again

Chronic pyelonephritis

• Repeated infections → scarring: small, echogenic kidney with cortical thinning and blunted calyces — the chronic rule (brighter + smaller), one more time

2The Pus Family

• Renal abscess — a pyelonephritis complication: complex fluid collection with thick walls, possibly containing gas. The tell: fever + leukocytosis persisting despite antibiotics
• Pyonephrosis — pus inside an OBSTRUCTED collecting system: hydronephrosis + internal echoes/debris/fluid levels. Fever + hydro = suspect pyonephrosis → urgent drainage
• Emphysematous pyelonephritis — gas-forming bacterial infection of the parenchyma, classically in diabetics: gas → dirty shadowing. A surgical emergency
• Fungal infections / fungus balls — Candida in immunocompromised patients, diabetics, or long-term catheters: echogenic, NON-shadowing, mobile masses in the collecting system

3Renal Failure

Sorted by where the problem lives:

• Prerenal — hypoperfusion before the kidney: CHF, shock, dehydration
• Intrinsic (renal) — the kidney itself: acute tubular necrosis (ATN) is the most common cause of acute renal failure — from toxins or ischemia; also glomerulonephritis
• Postrenal — obstruction after the kidney: the one ultrasound OWNS

• Chronic renal failure — most common causes: diabetes + hypertension
• End-stage kidneys: small (<8–9 cm), echogenic, thin cortex, loss of corticomedullary differentiation
• Management: hemodialysis or peritoneal dialysis → recall the dialysis kidneys develop acquired cystic disease with elevated RCC risk — monitor them

4The Renal Transplant

• Placed superficially in the iliac fossa (usually RLQ) — shallow enough for a higher-frequency transducer than native kidneys
• A normal transplant looks like a normal kidney, often slightly larger than a native one
• The native kidneys stay in place and atrophy

Complications

• Rejection — enlarged transplant, enlarged hypoechoic pyramids, decreased sinus fat visibility
• ATN — the first days post-op, from ischemia between harvest and transplant; usually recovers
• Obstruction — hydronephrosis of the transplant

Peritransplant fluid collections — the timeline is the answer

• Hematoma — EARLY, immediately post-op (blood, mixed echoes)
• Urinoma — EARLY, from a urine leak at the anastomosis
• Lymphocele — LATER (weeks to months), the MOST COMMON peritransplant collection; typically medial
• Abscess — any time infection strikes: fever + complex collection

5The Urinary Bladder

• Normal distended wall: ≤3 mm; scan through a comfortably full bladder
• Cystitis — bladder infection (females more often): diffusely thickened wall, sometimes debris in the urine
• Bladder diverticula — outpouchings of the wall; trapped urine stagnates → infection and stones
• Ureterocele — cystic dilation of the distal ureter ballooning into the bladder — the “cobra head”
• Post-void residual — measure what remains after voiding; a minimal residual is normal, large residuals mean retention
• Pitfall: a Foley catheter balloon is a round anechoic structure in the bladder — not a cyst, not a mass

1Anatomy & Location

The spleen is an INTRAPERITONEAL organ in the left upper quadrant (the left hypochondriac region), fully protected by the lower left rib cage — which is exactly why it must be scanned intercostally.

• Neighbors: inferior and anterior to the diaphragm · posterior to the stomach · lateral to the pancreatic tail, left kidney, left adrenal, and the splenic flexure of the colon
• Two surfaces: the smooth convex diaphragmatic surface facing the diaphragm, and the visceral surface molded to the stomach, left kidney, and colic flexure
• Hilum — on the medial aspect: entry/exit for the splenic artery, splenic vein, lymphatics, and nerves

2Vasculature — the Celiac Connection

• The celiac axis is the FIRST branch of the abdominal aorta, dividing into three vessels: the common hepatic artery (liver), the left gastric artery (stomach), and the splenic artery (spleen)
• The SMA sits just inferior to the celiac axis, feeding the intestines
• The splenic vein exits the hilum, runs posterior to the pancreatic tail and body, and joins the SMV at the portal-splenic confluence → main portal vein

3Physiology — Red Pulp, White Pulp

• Red pulp — the filter: macrophages phagocytose old red blood cells, bacteria, and foreign particles, cleaning the blood before returning it
• White pulp — the immune arm: lymphocytes that recognize, fight, and remember invaders; the spleen also initiates antibody production and makes plasma cells
• Blood reservoir — ~200 mL held in the venous sinuses, released during emergencies like internal bleeding
• In embryonic life the spleen makes red blood cells; bone marrow takes over in adults

4Lab Values

• Hematocrit — % of red cells vs. plasma volume · Hemoglobin — the oxygen-transport protein · RBC count
• WBC count — an elevated count always means infection or malignancy somewhere in the body
• CBC — counts everything, including platelets
• Platelets — the clotting number. High: malignancy, post-splenectomy, acute infection, polycythemia vera. Low: anemia — and a major procedure concern

5Size & Congenital Variants

• Accessory spleen — the most common variant: an extra nodule of splenic tissue, usually <1 cm, near the hilum or pancreatic tail, isoechoic to the spleen. Clinically meaningless — but it can impersonate a lymph node or a pancreatic-tail/renal mass. Uncertain? CT with contrast settles it
• Asplenia — congenital absence; extremely rare, associated with congenital heart disease; immunocompromised from birth
• Polysplenia — more than one spleen; rare
• Splenic cleft — a harmless groove in the surface
• Ectopic (wandering) spleen — out of its LUQ home; risk is torsion cutting off the blood supply. Located by nuclear medicine — the sonographer's job is only to document “spleen not visualized in the LUQ, patient denies surgical removal”, not to hunt for it

6Ultrasound Appearance & the 4-Image Protocol

• Normal look: uniform, homogeneous, medium-level echoes — isoechoic or slightly hypoechoic to the liver; smooth surface; the echogenic left hemidiaphragm caps it superiorly; anechoic tubes at the hilum = splenic vessels
• The whole protocol is FOUR images: sagittal/coronal with measurements (cranial-caudal + AP), sagittal without, transverse with (width), transverse without

Technique

• NPO 8–12 hours; almost never scanned alone — exceptions: trauma (splenic rupture) and pediatric mono with splenomegaly
• Best position: RLD with the left arm raised overhead — opens the intercostal spaces
• Probe intercostal in the inferior left interspace; poor view → move up one rib space; deep breath only if it isn't showing
• Coronal + transverse planes, low-frequency curved transducer

Pitfalls

• The left liver lobe crossing midline mimicking a splenic abnormality
• The spleen sitting behind/lateral to the left kidney read as a renal mass
• Adrenal or pancreatic-tail tumors — and a fluid-filled stomach — impersonating splenic masses. Know the anatomy before drawing conclusions

1Splenomegaly

>13 cm superior-to-inferior = enlarged. A common, often non-specific finding — ultrasound can't always name the cause.

• Other causes: congestion (heart failure, portal/splenic vein clots, cystic fibrosis), infections (hepatitis, mono, HIV), neoplasms (leukemia, lymphoma, mets), blood disorders (anemia), immune disease (lupus, RA), trauma, dialysis, metabolic/storage disease
• Sono clues: the spleen won't fit in the frame; a dilated splenic vein at the hilum; possible pleural effusion above the diaphragm; hypoechoic lesions throughout if lymphoma is the driver

2Infarct & Abscess

Splenic infarct

• Blood supply cut off — usually an embolus from the heart lodging in the splenic artery; classic with bacterial endocarditis (IV drug users); also leukemia, atherosclerosis, pancreatitis, cancers
• Acute: LUQ pain · chronic: often silent
• Sono: well-defined, WEDGE-shaped, base toward the capsule — early infarcts hypo-/isoechoic, aging into echogenic scar

Splenic abscess

• Uncommon but high mortality — usually diagnosed late; caused by sepsis (bacteroids, enterococci, strep, staph, salmonella, E. coli)
• ALWAYS fever + leukocytosis (elevated WBC — the infection rule from Lesson 14); LUQ pain, sometimes chest/left shoulder pain from diaphragm pressure
• Sono: variable — hypoechoic with low-level echoes, shaggy borders, mixed echogenicity, dirty shadowing if gas is inside. Can resemble a hematoma or degenerating neoplasm — clinical correlation decides

3Cysts, Trauma & Calcifications

Splenic cysts

• True cysts — epithelial-lined, uncommon: 90% dermoid, 10% epidermoid; usually solitary and unilocular
• Secondary cysts — pseudocysts, hemorrhagic cysts, abscesses; may have calcified walls (bright rings)
• The usual cyst look: anechoic, clean borders, posterior enhancement; fluid-fluid levels or thick borders suggest infection/hemorrhage

Splenic trauma

• Blunt LUQ injury — common, especially in children (MVAs, sports, wounds, abuse); spontaneous rupture can strike a spleen weakened by mono, malaria, or portal hypertension
• Intracapsular bleeding — blood contained within the capsule: enlarged spleen with hypo-/iso-/hyperechoic areas by hematoma age
• Capsular rupture — blood escapes: free fluid in the pericolic gutters, Morrison's pouch, posterior cul-de-sac. LUQ pain, rigidity, shock — a surgical emergency

Calcifications

• Echogenic foci ± shadowing — most commonly healed granulomas from histoplasmosis or TB (liver and lungs may join in); also arterial/aneurysm calcification, old infarcts, old hematomas, calcified cyst walls
• Generally harmless — recognize and document, don't diagnose the cause

4Splenic Neoplasms

Benign

• Hemangioma — the most common benign splenic neoplasm: small, often silent, hyperechoic-to-mixed
• Hamartoma — always benign anywhere; rare in the spleen; lymphoid tissue; echogenic and well-defined
• Cavernous lymphangioma — lymphatic malformation, hemangioma look-alike
• Benign masses are left alone once confirmed — but ultrasound can't confirm; biopsy does

Malignant

• Angiosarcoma (hemangiosarcoma) — rare primary splenic malignancy; patients often anemic; looks like a hemangioma; metastasizes to the liver
• Lymphoma — Hodgkin's or non-Hodgkin's: hypoechoic lesions, splenomegaly optional; the spleen is immune tissue, so lymphoma finds it often
• Metastases — arrive late in disease; most common primary: MELANOMA; also lung, breast, colon, ovary; variable look including the target/bullseye sign (same as liver mets)

5The Anterior Abdominal Wall

• Abscess — post-surgery/injection; most common in the rectus muscle; variable look; always fever + elevated WBC
• Hernia — intestine protruding through a wall defect (anterior, inguinal, femoral): a break in the wall's symmetry with peristalsis inside the sac — moving bowel content is the giveaway. Deep hernias → CT. Surgical repair typical
• Lipoma — benign fatty tumor; looks like the surrounding fat with visible borders; soft and mobile
• Desmoid tumor — benign myofibroblastic growth, often from surgical scar tissue, embedded in the wall muscles; soft, mobile, never malignant
• Malignant mets (melanoma, breast) — rare; the clinical tell: FIRM and NON-mobile

1The Pediatric Approach

• Higher-frequency, small-footprint transducers — less tissue depth to penetrate
• Trust first: eye contact, soft voice, lights on, let the child touch the probe and feel the warm gel; skip the white coat
• By age: infants — feed during the exam or parent holds · 2–4 — distract with toys · 5–7 — coach breath-holds · older kids — show and explain
• Crying patient? Capture between breaths with the cine loop. Hard-to-localize mass? Drape the child prone over a parent's lap to separate structures

2Pediatric Liver Pathology

• Hepatitis — B more than A in kids; ↑ALT/AST; ultrasound assesses damage, it doesn't diagnose hepatitis
• Wilson's disease — inherited copper metabolism disorder: copper piles up in the liver, leaks to the brain; hallmark Kayser-Fleischer ring (brownish-green ring around the iris); treated with penicillamine; sono ranges hepatomegaly → cirrhosis
• Reye's syndrome — aspirin + viral infection (chickenpox, flu), ages 3–16: vomiting, lethargy, confusion → seizures/coma; sono: echogenic (fatty) liver, possible hepatomegaly, NO jaundice
• Mesenchymal hamartoma — rare benign tumor, ≤2 years, embryonal tissue, nonspecific well-circumscribed look

• Mets remain the most common liver malignancy overall — in children the top primary sources are neuroblastoma and Wilms tumor
• Neonatal hepatosplenomegaly → think TORCH (Toxoplasmosis, Rubella, CMV, Herpes, Syphilis) + HIV — placenta-crossing infections; may bring microcephaly and calcifications

3Biliary Anomalies — the Atresia Emergency

• Caroli's disease and choledochal cysts — the Lesson 7 pair, revisited from the pediatric side: string-of-beads intrahepatic dilation; porta-hepatis cyst with pain, intermittent jaundice, palpable RUQ mass
• Biliary atresia — the bile ducts from liver to duodenum are obliterated: persistent newborn jaundice, dark urine, hepatomegaly, acholic (pale) stools

4Pediatric Urinary Tract

• Infant kidney recap (Lesson 10): cortex iso/hyperechoic to liver, big prominent pyramids (not cysts), less echogenic sinus, lobulated contour; measure against age-appropriate charts
• UPJ obstruction — the most common cause of pediatric hydronephrosis, more in male infants
• Posterior urethral valves (PUV) — the most common bladder outlet obstruction in male infants: redundant urethral tissue folds → distended thick-walled bladder, dilated ureters, hydro — and the signature “keyhole” (dilated bladder + proximal urethra)
• Infantile polycystic kidney disease (ARPKD) — bilateral, enlarged, echogenic, non-functioning — not compatible with life (Lesson 11's story)
• Wilms tumor — most common pediatric renal malignancy, ages 2–5: large often-silent flank mass, solid hyperechoic to inhomogeneous with hemorrhage/necrosis; aggressive — spreads to liver, lungs, brain; aggressive chemo

5Pediatric Adrenal Pathology

• Neuroblastoma — malignant adrenal tumor, 2 months–4 years: highly aggressive, often already metastatic at diagnosis; the anatomical neighbor problem: hard to distinguish from Wilms tumor. Associations: Beckwith-Wiedemann, Klippel-Feil, fetal alcohol syndrome, Hirschsprung's
• Neonatal adrenal hemorrhage — most commonly 2–7 days after birth (fetal stress, anoxia, birth trauma, bleeding disorders, maternal diabetes, sepsis): a complex hypoechoic or mixed cystic-solid mass beside the kidney. Neonatal adrenals are proportionally big — thick echogenic medulla, hypoechoic cortex

6The GI Tract & Appendicitis

• Bowel basics: gas = dirty shadowing; fluid-filled loops mimic cysts, feces mimic tumors — peristalsis in real time separates bowel from everything else; bowel shows the target/bullseye pattern
• Appendicitis clinical: periumbilical pain migrating to the RLQ, nausea, anorexia, fever, WBC >10,000 — and a positive McBurney's point (rebound tenderness: pain returns on release)
• Technique: transverse from above the umbilicus, slide inferior with graded compression

7Lymph Nodes — the Hilum Rule

• Normal abdominal/pelvic nodes: <1 cm, usually invisible; para-aortic chain rings the aorta/IVC; regional nodes at the porta hepatis, mesentery, iliacs
• Hodgkin's — under 30, high cure rate · non-Hodgkin's — over 40, lower cure rate; both: fevers of unknown origin, night sweats, weight loss

1Thyroid Anatomy

• A butterfly-shaped gland in the anterior neck: a right lobe and left lobe on either side of the trachea, joined across the midline by the isthmus, which drapes directly anterior to the trachea
• Mild asymmetry is normal — the right lobe is often the larger one
• Tends to be larger in women, and grows with hormonal shifts: puberty, pregnancy, lactation, and phases of the menstrual cycle

2The Neighborhood

• Major neurovascular bundle (lateral): common carotid artery, internal jugular vein, and vagus nerve
• Minor neurovascular bundle (posterior to each lobe): inferior thyroid artery and recurrent laryngeal nerve
• Anterior muscles: the thin strap muscles (sternohyoid, sternothyroid) lie directly over the gland; the larger sternocleidomastoid sits anterolaterally
• Longus colli — deep, posterior to each lobe, against the spine
• Esophagus — just left of midline, posterior and medial to the left lobe
• Trachea — always midline; its cartilage is bright and casts a posterior shadow

• Arterial supply: the superior thyroid artery (first branch of the external carotid) and the inferior thyroid artery
• Venous drainage: mainly into the internal jugular vein

3Thyroid Physiology & Labs

• An endocrine gland: it makes, stores, and releases hormones that set metabolic rate, heart rate, and how fast the body burns calories
• The chain of command: the pituitary releases TSH → the thyroid makes T4 (thyroxine) → T4 converts to T3 (triiodothyronine), the active form inside cells
• Iodine is stored in the thyroid and is required to build T3 and T4 — too little dietary iodine can cause a goiter
• Calcitonin — a third thyroid hormone; it lowers blood calcium (the counterweight to PTH)
• A thyroid panel checks TSH, T3, and T4. They usually move in opposite directions: high TSH with low T3/T4, or low TSH with high T3/T4
• After a total thyroidectomy, the patient takes hormone replacement for life

4The Parathyroid Glands

• Four tiny glands, under 5 mm each, in two pairs behind the upper and lower poles of the thyroid
• Neighbors only — they are functionally unrelated to the thyroid
• They make parathyroid hormone (PTH), which controls serum calcium
• Too much PTH pulls calcium out of bone → osteoporosis over time, plus hypercalcemia that strains the kidneys → recurrent kidney stones and, in long-standing cases, medullary calcifications (nephrocalcinosis)
• Normal glands are usually not seen. In very thin patients they may show as small, flat, hypoechoic structures behind the thyroid

5Congenital Variants

• Pyramidal lobe — a finger of thyroid tissue extending superiorly from the isthmus, usually just left of midline; isoechoic to the rest of the gland; present in roughly 40–50% of people — a normal variant, not a mass
• Ectopic thyroid — thyroid tissue outside its normal position; about 90% is lingual (at the base of the tongue); located with other imaging such as a nuclear medicine scan or CT
• Ectopic parathyroid — glands sitting higher or lower than expected, or rarely in the mediastinum; not a routine ultrasound evaluation

6Why the Exam Gets Ordered

• Palpable neck mass — felt in the thyroid region or lateral neck
• Cold nodule on a nuclear medicine scan — a non-functioning, photon-deficient area. A single cold nodule carries a real malignancy risk (often quoted around 20%), and ultrasound's job is to show whether it is cystic or solid
• Abnormal T3/T4 on blood work
• Elevated serum calcium — searching for a parathyroid adenoma

7Normal Sonographic Appearance

• Homogeneous, medium-level (mid-gray) echoes through both lobes and the isthmus, with smooth borders
• More echogenic than the surrounding muscles
• Small anechoic tubes inside the gland are its arteries and veins — color Doppler confirms them and shows the gland's rich flow

8Scanning Technique & Protocol

• Prep: none
• Position: supine with the neck hyperextended — pillow under the shoulders or a rolled towel under the neck. Can't extend (a stiff elderly neck)? Turn the head slightly away from the side being scanned
• Ask the patient to avoid swallowing while you capture images — swallowing moves the gland
• Transducer: high-frequency linear, ideally ~15 MHz (7.5–10 MHz minimum). Save the curved probe for very large necks or goiters
• Start between the Adam's apple and the sternal notch

• Image both lobes and the isthmus in sagittal and transverse
• Label every image right or left — sagittal thyroid views have no landmark that tells the sides apart
• Finish the full protocol first, then add images of any pathology
• Note patient limitations (for example, can't move the neck) in the report when image quality suffers

1Thyroid Function Gone Wrong

• Hypothyroidism is treated with daily oral thyroid hormone (levothyroxine)

2Thyroid Nodules (Adenomas)

• Benign solid growths of the follicular tissue — the most common thyroid mass
• Often multiple. A single, dominant nodule deserves a closer look — cancer tends to be solitary
• Most need no treatment unless they make enough hormone to cause hyperthyroidism, or their size and features call for a biopsy
• Sono: usually hypoechoic, but can be iso-, hyperechoic, or complex; often ringed by a thin hypoechoic halo
• Degenerating nodules outgrow their blood supply → cystic areas, debris, calcifications, septations

3Goiters

• Goiter = enlargement of the thyroid
• Non-toxic goiter — from iodine deficiency; more common in females, often around puberty; smooth, homogeneous, diffusely enlarged; thyroid function stays normal
• Toxic diffuse goiter (Graves' disease) — autoimmune; the whole gland is enlarged and hypoechoic, with hyperthyroid symptoms and sometimes exophthalmos (bulging eyes)
• Multinodular goiter — many nodules enlarging the gland; ages 50–70, more common in females, runs in families; heterogeneous with discrete nodules and cystic degeneration

4Hashimoto Thyroiditis

• A chronic autoimmune inflammation — the immune system's lymphocytes gradually destroy the gland
• The most common cause of hypothyroidism; most often middle-aged women
• Sono: enlarged, heterogeneous, coarse texture, often hypervascular; small nodules and calcifications may appear

5Thyroid Cancer

• Uncommon and highly treatable — a very small share of cancer deaths
• Papillary — the most common (60–70%); slow-growing; ages 40–60; twice as common in women; may spread to neck lymph nodes but is rarely fatal
• Follicular — also slow, but more aggressive than papillary; spreads through the bloodstream over time
• Medullary — more aggressive than papillary or follicular; typically ages 50–60; arises from the calcitonin-making cells and can run in families
• Risk factors: prior radiation to the neck, especially in childhood, including radiation treatment for another cancer

6Ultrasound-Guided FNA Biopsy

• Who does what: the radiologist inserts the needle. The sonographer handles consent, patient prep, room and sterile tray setup, finding the nodule, running the machine, and aftercare instructions
• Needle: fine, usually 25 or 27 gauge
• Local anesthetic: 1% lidocaine with epinephrine
• Several passes with separate needles — typically some for cytology and some for molecular (gene expression) testing
• A lab technician often checks sample adequacy in the room

7Cystic Neck Masses (Not Thyroid)

8Parathyroid Adenoma

• Benign tumor, typically 8–15 mm, making excess PTH → hyperparathyroidism and high serum calcium
• Consequences: kidney stones, medullary calcifications, weakened bones and bone cysts
• Sono: a well-defined hypoechoic oval posterior and deep to the lower pole of the thyroid
• Normal parathyroids aren't seen — an adenoma is what makes one visible. Thyroid and parathyroid are scanned together

9Other Imaging

• Ultrasound is the first-line exam for the thyroid
• MRI gives the best soft-tissue detail after ultrasound; CT is useful but less detailed; plain X-ray has little role
• Nuclear medicine sorts nodules by function:

1The Six Layers (Superficial → Deep)

• The nipple holds the openings of the lactiferous ducts (about 15–20 duct systems). The areola holds Montgomery glands — normal sebaceous glands, not lesions
• The retromammary fat looks more prominent in older, obese, and pregnant patients

2The Mammary Layer — Where Pathology Lives

• The functional (glandular, parenchymal) layer: 15–20 lobes, each made of lobules; lobules contain the milk-producing acini
• The terminal duct lobular unit (TDLU) — the lobule plus its terminal duct — is where most breast pathology, including most cancers, begins
• Cooper's ligaments — thin bright linear bands that support the breast
• Lactiferous ducts — anechoic/hypoechoic tubes that look like vessels but show no color flow
• The tail of Spence (axillary tail) extends breast tissue up into the axilla

3Development & Anomalies

• Breast tissue starts forming in the 4th week of embryonic life along the milk line, which runs from the axilla to the groin
• In males, testosterone stops further development — a nipple and minimal tissue remain
• Newborns can have temporary breast swelling from maternal hormones
• Anomalies: amastia (no breast) · polymastia (extra breast) · athelia (no nipple) · polythelia (extra nipple — the most common)

4Hormones & Life Stages

• Puberty: estrogen and progesterone from the ovaries grow the breast
• Menstrual cycle: cyclic changes, including premenstrual swelling
• Lactation: prolactin makes the milk; oxytocin lets it flow (let-down). Milk moves from the acini through progressively larger ducts to the lactiferous sinus and out the nipple. Ducts return to normal size about 3 months after breastfeeding stops
• Menopause: involution — glandular tissue is replaced by fat, so the mammary layer thins

5Why Breast Ultrasound Gets Ordered

• Follow-up of an abnormal mammogram — the most common indication. Screening mammograms typically start at age 40; an abnormal screen leads to a diagnostic mammogram, then targeted or whole-breast ultrasound
• Dense breasts — lesions can hide from mammography in dense tissue
• Under 30 with a lump or pain — ultrasound comes first
• Pregnant or breastfeeding — ultrasound is first-line; mammography is generally avoided
• Men — men get breast cancer too
• Axillary evaluation when a suspicious solid mass is found

6Scanning Technique

• Position: supine, arm on the side being scanned raised above the head, nipple pointing at the ceiling. Large breasts: roll into an oblique or decubitus position with a pillow under the shoulder. Occasionally sitting or standing
• Transducer: the highest frequency linear that still reaches the chest wall — typically 9–15 MHz, as low as ~7 MHz for large breasts
• Multiple focal zones work well because breast tissue barely moves
• The inframammary fold (IMF) — where the underside of the breast meets the chest wall — is a landmark you'll see referenced in orders

7Labeling & Exam Types

• Quadrants: upper outer · upper inner · lower inner · lower outer · plus retroareolar (behind the nipple). The upper outer quadrant holds the most tissue and the most cancers
• Clock face: the breast as a clock, viewed facing the patient, plus the distance from the nipple in cm — e.g., “Right breast, 2:00, 3 cm from the nipple”
• Whole-breast exam: the entire breast scanned and documented per protocol · Targeted exam: only the area of concern, in multiple planes
• Exact protocols vary by facility and radiologist

1The Organs

• Primary sex organs: the testes — ovoid glands that make sperm
• Accessory sex organs: epididymis, ductus (vas) deferens, seminal vesicles, prostate, bulbourethral glands, scrotum, and penis — they protect, carry, and nourish sperm, and all can be imaged with ultrasound
• The scrotum is a two-compartment pouch split by the median raphe. Each side holds a testis, an epididymis, and the lower spermatic cord
• The testes sit outside the body because sperm production needs a temperature about 2–3 degrees cooler than the core

2Coverings & the Mediastinum Testis

• Tunica albuginea — the thin, tough fibrous capsule directly around each testis
• Tunica vaginalis — a two-layered sac around the front and sides of the testis. A small amount of fluid between its layers is normal; too much is a hydrocele
• The tunica albuginea folds inward at the back of the testis to form the mediastinum testis, with thin septa fanning out into the gland

3Inside the Testis & the Sperm Pathway

• Lobules packed with seminiferous tubules, where sperm form (spermatogenesis)
• Sertoli cells in the tubules nurture developing sperm
• Leydig cells between the tubules make testosterone
• Exocrine job = sperm (leaves the body) · Endocrine job = testosterone (stays in the body)

• The epididymis is a coiled tube curving along the back and side of the testis: head (globus major) at the upper pole, body, and tail at the lower pole
• The head is the easiest part to see and is routinely measured; measure the body and tail only if enlarged

4Development

• The testes form in the abdomen near the kidneys and descend into the scrotum late in fetal life, usually by about the 8th month
• Because the two systems develop side by side, an anomaly in one often comes with an anomaly in the other

• Polyorchidism — an extremely rare duplication, usually three testes (two on one side); more often on the left; shown in transverse, confirmable with MRI

5Blood Supply & the Spermatic Cord

• Veins: the pampiniform plexus — a web of small veins draining the testis — merges into the spermatic (testicular) vein
• Right spermatic vein → IVC · Left spermatic vein → left renal vein
• Spermatic cord = testicular artery + spermatic veins + ductus deferens (plus nerves and lymphatics), running up through the inguinal canal

6Normal Appearance & Measurements

• Testes: homogeneous, mid-level gray — a lot like the thyroid. Both sides should match in size and echogenicity
• Epididymis: similar echogenicity to the testis; the head is easiest to find

7Why It Gets Ordered: Torsion

• Testicular pain — especially in the ER — almost always means a scrotal ultrasound to rule out torsion: the testis twists and cuts off its own blood supply
• It's a surgical emergency — the sooner flow is restored, the better the chance of saving the testis

8The Scrotal Protocol

• Setup: patient undressed from the waist down under a sheet; a towel lifts the penis onto the abdomen, another towel under the scrotum as a shelf. Scan with your arm under the sheet to protect privacy
• Transducer: high-frequency linear, ideally ~15 MHz (around 12 MHz for a swollen scrotum)
• Color settings: testicular flow is slow, so keep the velocity scale low — a scrotal preset usually does this

• Sagittal through each testis: medial, mid, lateral
• Transverse through each testis: upper pole, mid, lower pole
• Measure length, width, and height of each testis, plus the epididymal head
• Color and spectral Doppler of arterial and venous flow in each testis — always
• Spermatic cord in the inguinal canal; check for a varicocele with Valsalva

1Course & Wall of the Aorta

• The aorta enters the abdomen through the aortic hiatus of the diaphragm at about T12 and becomes the abdominal aorta
• It runs retroperitoneally, anterior to the spine and slightly left of midline, tapering as it gives off branches
• It bifurcates into the right and left common iliac arteries at about L4, roughly the level of the umbilicus
• The IVC lies to the right of the aorta; on a transverse image (patient's right on screen left) the IVC is on the screen left, the aorta on the screen right

Three layers of the wall

• Tunica intima: the inner endothelial lining, in contact with blood
• Tunica media: the middle layer of smooth muscle and elastic tissue; thickest in arteries
• Tunica adventitia (externa): the outer connective-tissue layer

2Branches in Order

• Celiac axis (trunk): the first anterior branch, about 1–2 cm below the diaphragm. A short trunk (roughly 1–2 cm) that trifurcates into the common hepatic, splenic, and left gastric arteries
• Superior mesenteric artery (SMA): the second anterior branch, about 1 cm below the celiac. It runs inferiorly, parallel to the aorta, and supplies the small bowel and right/proximal colon
• Renal arteries: lateral branches just below the SMA. The right renal artery passes posterior to the IVC
• Inferior mesenteric artery (IMA): a small anterior/left branch at about L3, a few centimeters above the bifurcation; often hard to see
• Bifurcation into the common iliac arteries at about L4. Each common iliac divides into internal and external iliac arteries
• Smaller branches (inferior phrenic, middle suprarenal, gonadal, lumbar, median sacral) are rarely seen on routine scans

3Measuring the Aorta

• Measure perpendicular to the long axis of the vessel, never on an oblique cut, which overestimates the diameter
• Outer wall to outer wall (adventitia to adventitia) is the commonly recommended method; some labs measure inner-to-inner, so follow the protocol and be consistent on follow-ups
• AP diameter in sagittal (or transverse) and transverse (width) in the transverse plane
• Standard levels: proximal (near the celiac/SMA), mid (near the renals), distal (just above the bifurcation), plus both common iliac arteries
• If an aneurysm is present, document its maximum diameter, length, its relationship to the renal arteries, and any extension into the iliacs

4Aortic Doppler

• Proximal (suprarenal) aorta: feeds the celiac and renal beds, which have low resistance, so the waveform shows more forward flow in diastole (lower resistance)
• Distal (infrarenal) aorta: feeds the resting legs, a high-resistance bed, so the waveform is triphasic: sharp systolic upstroke, brief flow reversal in early diastole, then a small forward component
• Normal flow is laminar with a clear spectral window. Turbulence and spectral broadening suggest stenosis or plaque; swirling flow is common inside an aneurysm

5Abdominal Aortic Aneurysm (AAA)

• Definition: an abdominal aortic diameter of 3 cm or more, or 1.5 times the normal proximal segment
• Location: the large majority are infrarenal; always state whether the neck involves the renal arteries
• Shapes: fusiform (circumferential, spindle-shaped; the most common) vs saccular (an outpouching from one side)
• Mural thrombus is common: low-level echoes lining the wall, often eccentric. Measure the whole aneurysm wall to wall, not just the residual lumen
• Risk factors: smoking, male sex, age over about 65, hypertension, atherosclerosis, family history
• Symptoms: often none; sometimes a pulsatile abdominal mass, abdominal or back pain

Growth, repair, and rupture

• Rupture risk rises with diameter. Elective repair is commonly considered at about 5.5 cm in men (often somewhat smaller in women), with rapid growth (about 1 cm per year or more), or when the aneurysm is symptomatic
• Signs of rupture: sudden severe abdominal, back, or flank pain, hypotension, and a pulsatile mass; a falling hematocrit. Rupture usually bleeds into the retroperitoneum, seen as a hypoechoic or complex periaortic/retroperitoneal hematoma
• Ultrasound can show an AAA and a hematoma, but CT is the test of choice for suspected rupture in a stable patient; an unstable patient goes to surgery

6Dissection, Pseudoaneurysm & Ectasia

Aortic dissection

• A tear in the intima lets blood track into the media, splitting the wall into a true lumen and a false lumen
• Sonographic hallmark: a thin, linear, mobile intimal flap that moves with the cardiac cycle
• Color Doppler often shows different flow in each lumen. The false lumen may have slow flow or thrombose. The true lumen is usually the smaller one and expands in systole
• Risk factors: hypertension (most common), Marfan syndrome and other connective tissue disorders, trauma. Classic symptom: sudden tearing chest or back pain
• Abdominal dissections are usually an extension from the thoracic aorta; CT angiography is the main diagnostic test

True aneurysm vs pseudoaneurysm

• Ectasia: diffuse dilation of the aorta that does not reach aneurysm criteria (under 3 cm and less than 1.5 times normal), often with tortuosity in older patients

7EVAR Follow-Up & Endoleaks

• EVAR (endovascular aneurysm repair) places a stent graft inside the aneurysm through the femoral arteries. The graft excludes the sac from circulation
• Follow-up imaging checks sac diameter (should stay stable or shrink), graft position and patency, and looks for endoleak: persistent flow inside the sac but outside the graft
• A growing sac after EVAR is a warning sign even when no leak is seen

8The Inferior Vena Cava

• Formed by the union of the common iliac veins at about L5, slightly below the aortic bifurcation
• Runs right of midline, retroperitoneal, passes through the caudate/posterior liver groove, pierces the diaphragm at the caval hiatus (about T8), and empties into the right atrium

Tributaries (inferior to superior)

• Common iliac veins → lumbar veins → right gonadal vein → renal veins → right suprarenal (adrenal) vein → inferior phrenic veins → hepatic veins
• On the left, the left gonadal and left adrenal veins drain into the left renal vein, not directly into the IVC
• The left renal vein is longer than the right and crosses anterior to the aorta, posterior to the SMA

• Doppler: near the heart the IVC waveform is pulsatile, reflecting right atrial pressure changes (similar to the hepatic veins). Farther from the heart it becomes more phasic with respiration

IVC pathology

• Bland thrombus: echogenic material in a distended, non-compressible lumen with a filling defect on color; often extends up from the iliac/leg veins
• Tumor extension: renal cell carcinoma is the classic tumor to grow through the renal vein into the IVC, sometimes up to the right atrium. Others: hepatocellular carcinoma (via hepatic veins), adrenal carcinoma, Wilms tumor in children
• Tumor thrombus may show internal vascularity with arterial waveforms; bland thrombus does not. Always trace the renal vein and IVC when a renal mass is found
• IVC filters are placed, usually infrarenal (just below the renal veins), to trap emboli in patients with DVT who cannot take anticoagulation. They appear as bright linear echoes in the lumen; check for thrombus above and below and for tilt or migration

9Scanning Technique

• Prep: NPO for about 6–8 hours (often overnight; scheduled in the morning) to reduce bowel gas. An emergency exam is never delayed for prep
• Transducer: low-frequency curved array, about 2–5 MHz; a phased array helps between ribs or in tight windows
• Position: supine to start; add decubitus positions when gas is in the way
• Sequence: sagittal and transverse from the diaphragm to the bifurcation, then each common iliac; measure proximal, mid, and distal; add color and spectral Doppler as indicated
• For the IVC: sagittal and transverse from the right atrium to the iliac confluence, with a sniff or respiratory cine clip when asked to assess collapsibility

1The Portal Venous System

• The main portal vein (MPV) forms at the portal confluence, where the superior mesenteric vein (SMV) joins the splenic vein, posterior to the neck of the pancreas
• The inferior mesenteric vein (IMV) usually drains into the splenic vein (sometimes the SMV or the confluence)
• The MPV runs up through the porta hepatis in the hepatoduodenal ligament and divides into the right and left portal veins
• The portal vein brings about 70–75% of the liver's blood supply (nutrient-rich gut blood); the hepatic artery brings the rest, but about half of the oxygen

Normal portal flow

• Hepatopetal = flow toward the liver (normal). Hepatofugal = flow away from the liver (abnormal)
• Waveform: monophasic and continuous, with gentle respiratory phasicity (a mild undulation, sometimes slight cardiac pulsatility)
• Normal MPV velocity is commonly quoted as about 15–40 cm/s. Velocity and diameter increase after a meal
• Normal MPV diameter is typically ≤13 mm in quiet respiration

2Hepatic Veins & Hepatic Artery

Hepatic veins: triphasic

• The right, middle, and left hepatic veins drain into the IVC just below the right atrium, so they reflect right-heart pressure changes. That is why the waveform is pulsatile
• Normal waveform is triphasic, with four components:
  • a wave: atrial contraction pushes blood briefly back into the liver (reversed, above baseline on a standard display)
  • S wave: ventricular systole; the tricuspid annulus moves toward the apex and the atrium fills, so flow runs toward the heart (largest antegrade wave)
  • v wave: atrium overfills just before the tricuspid valve opens; a small transition near or above baseline
  • D wave: ventricular diastole; the tricuspid valve opens and flow runs toward the heart again
• Loss of phasicity (flat, monophasic): cirrhosis (stiff liver), Budd-Chiari, or compression
• Increased pulsatility: tricuspid regurgitation (S wave becomes reversed) and right heart failure

Hepatic artery: low resistance

• The proper hepatic artery feeds a low-resistance organ: brisk systolic upstroke and continuous forward diastolic flow
• Normal RI is typically about 0.55–0.7
• When portal inflow falls (cirrhosis, portal vein thrombosis), the hepatic artery often enlarges and speeds up to compensate (the hepatic arterial buffer response)

3Portal Hypertension

• Increased resistance to portal flow raises portal pressure. Causes are grouped by level:
  • Prehepatic: portal or splenic vein thrombosis, extrinsic compression
  • Intrahepatic: cirrhosis (by far the most common cause)
  • Posthepatic: Budd-Chiari, right heart failure, constrictive pericarditis

Sonographic signs

• Dilated MPV > 13 mm; splenic vein and SMV may also enlarge
• Loss of respiratory variation in the portal, splenic, and SMV signals
• Low portal velocity, then to-and-fro flow, and finally hepatofugal (reversed) flow in advanced disease
• Splenomegaly, ascites, and portosystemic collaterals
• An enlarged, high-velocity hepatic artery is common as arterial inflow compensates

Portosystemic collaterals

4Portal Vein Thrombosis & Cavernous Transformation

• Causes: cirrhosis, hepatocellular carcinoma (HCC), pancreatitis and other abdominal inflammation, hypercoagulable states, trauma, and surgery
• Findings: echogenic material in the lumen with absent or reduced color flow. An acute clot can be nearly anechoic, so always confirm patency with color, power, and spectral Doppler at low flow settings
• Partial thrombus shows color flow passing around the clot

Cavernous transformation

• After chronic occlusion, many small periportal collateral veins form around the thrombosed portal vein, typically over weeks to months
• Appears as a tangle of tortuous, wormlike channels in the porta hepatis with hepatopetal flow; the original portal vein may not be identifiable

5Budd-Chiari Syndrome

• Obstruction of hepatic venous outflow: the hepatic veins, the IVC above them, or both
• Causes: hypercoagulable states (e.g., polycythemia vera, oral contraceptives, pregnancy), tumor, and a membranous web in the IVC
• Classic triad: abdominal pain, hepatomegaly, ascites

Sonographic findings

• Hepatic veins not seen, narrowed, or filled with thrombus; absent, reversed, or flat (monophasic) hepatic vein flow
• Intrahepatic venous collaterals (often comma-shaped) linking hepatic veins
• Caudate lobe hypertrophy: the caudate drains directly into the IVC through its own small veins, so it is spared and enlarges
• Hepatomegaly, ascites, splenomegaly; portal flow may be slow or reversed

6TIPS Assessment

• TIPS (transjugular intrahepatic portosystemic shunt) = a stent through the liver connecting a portal vein (usually the right) to a hepatic vein (usually the right), lowering portal pressure
• Indications: recurrent variceal bleeding and refractory ascites
• A baseline Doppler exam is done soon after placement, then at follow-up intervals per protocol. Sample the portal (inlet) end, mid shunt, and hepatic (outlet) end, plus the MPV and intrahepatic portal branches

Expected normal findings

• Shunt velocities typically about 90–190 cm/s throughout the stent
• MPV velocity increases (blood is drawn toward the low-pressure shunt), flowing hepatopetal toward the stent
• Intrahepatic portal branches (right and left portal veins) typically flow hepatofugal, toward the shunt. That reversal is expected after TIPS

Commonly taught signs of dysfunction

• Shunt velocity typically < about 90 cm/s or > about 190 cm/s (focal stenosis), or a change of more than about 50 cm/s from the baseline exam
• Drop in MPV velocity compared with baseline (thresholds around 30 cm/s are often cited)
• Return of hepatopetal flow in the intrahepatic portal branches (they had flowed toward the shunt)
• Absent flow in the stent = occlusion; reversed flow in the draining hepatic vein; recurrent ascites or varices

7Mesenteric Arteries & Ischemia

• Celiac axis (trunk): first anterior branch of the aorta; branches into the common hepatic, splenic, and left gastric arteries (the "seagull" in transverse)
• SMA: arises about 1 cm below the celiac, runs anterior to the left renal vein and posterior to the pancreas

Mesenteric ischemia

• Chronic: usually atherosclerosis; collaterals protect the bowel, so symptoms typically appear when two or more of the three vessels (celiac, SMA, IMA) are significantly narrowed
• Classic history: postprandial pain ("intestinal angina"), fear of eating, and weight loss
• Acute: often an embolus to the SMA; a surgical emergency usually diagnosed with CT angiography
• Commonly taught criteria for ≥70% stenosis (fasting): SMA PSV ≥ about 275 cm/s; celiac PSV ≥ about 200 cm/s. End-diastolic criteria (SMA EDV > about 45 cm/s, celiac EDV > about 55 cm/s) are also used
• Reversed flow in the common hepatic artery suggests severe celiac stenosis or occlusion, with collateral filling from the SMA via the pancreaticoduodenal arcades and gastroduodenal artery

Median arcuate ligament syndrome (MALS)

• The median arcuate ligament of the diaphragm compresses the celiac axis, giving a hooked, upturned shape in sagittal
• Celiac velocity is elevated in expiration and falls toward normal with deep inspiration. Always sample in both phases

8Renal Artery Doppler: Technique & Normal

• Prep: fasting (often overnight or about 6–8 hours) to reduce bowel gas
• Origins: from an anterior transverse view of the aorta just below the SMA; the right renal artery passes posterior to the IVC
• Mid and distal arteries and hilum: a flank (lateral decubitus, coronal) approach, the "banana peel" view, puts the renal artery more parallel to the beam
• Angle ≤60°, parallel to the vessel wall; sample with a small gate and walk it through the whole artery
• Record aortic PSV at the level of the renal arteries for the ratio

• Normal renal artery: low resistance, rapid systolic upstroke, often a small early systolic peak, and continuous forward diastolic flow. PSV is typically under about 180 cm/s
• Intrarenal (segmental/interlobar) arteries: same low-resistance shape at lower velocity

9Renal Artery Stenosis

• Atherosclerosis: older patients, usually the origin or proximal third
• Fibromuscular dysplasia (FMD): typically young to middle-aged women, the mid to distal artery, with a "string of beads" look on angiography
• Clinical clue: renovascular hypertension, especially hard-to-control or new in a young patient; the affected kidney may be smaller

• Direct signs (at the stenosis) are most reliable but technically hard. Indirect signs (tardus-parvus downstream) help when the main artery can't be fully seen, but mostly appear with severe stenosis
• The RAR is less reliable when the aortic PSV is very low or very high (e.g., aortic disease or low cardiac output)

1GI Tract Anatomy

• Esophagus & GE junction: the distal esophagus passes through the diaphragm and joins the stomach at the gastroesophageal (GE) junction. On a sagittal view just left of midline it sits anterior to the aorta and posterior to the left lobe of the liver, often as a small target shape
• Stomach: cardia (at the GE junction) → fundus (dome, under the left hemidiaphragm) → body → antrum → pylorus (muscular sphincter into the duodenum). Folds of the inner wall are called rugae
• Duodenum (four parts, a C-loop around the pancreatic head):
  • 1st, superior: the duodenal bulb, the only part that is intraperitoneal
  • 2nd, descending: receives the CBD and pancreatic duct at the ampulla of Vater
  • 3rd, horizontal: crosses midline between the SMA (anterior) and the aorta (posterior)
  • 4th, ascending: ends at the ligament of Treitz (duodenojejunal flexure)
• Jejunum vs ileum: the jejunum (mostly left upper abdomen) has prominent circular folds, the valvulae conniventes, giving a feathery pattern; the ileum (mostly right lower) has fewer, smoother folds and ends at the ileocecal valve
• Colon: cecum (with the appendix) → ascending → hepatic flexure → transverse → splenic flexure → descending → sigmoid → rectum. Its wall pouches are haustra

2The Gut Signature

• With a high-frequency transducer, normal bowel wall shows five alternating layers, called the gut signature. Odd layers are echogenic; even layers are hypoechoic

Normal wall thickness

• Distended small bowel and colon: typically ≤3 mm
• Non-distended bowel, gastric antrum and pylorus: typically up to about 5 mm. Collapsed bowel always looks thicker, so judge thickness on a distended segment when you can

3Graded Compression & the Target Sign

• Transducer: start with a curved array survey, then switch to a high-frequency linear array (about 5–12 MHz) for bowel detail
• Graded compression: apply slow, steady, gradually increasing pressure. This displaces gas-filled loops and brings the bowel closer to the probe. Normal bowel compresses; an inflamed appendix or bowel loop does not
• Compress gradually, never abruptly: sudden pressure hurts a patient with peritonitis and causes guarding
• Ask the patient to point to the spot that hurts most and focus there. A probe-elicited tender spot over an abnormal structure is a helpful sign
• Peristalsis: watch each loop in real time; normal small bowel shows active peristalsis

Target and pseudokidney signs

• When the wall is thickened, a loop seen in transverse shows a target (bull's-eye, donut): a hypoechoic rim around an echogenic center of mucosa and lumen contents
• The same loop in long axis looks like a pseudokidney: a hypoechoic "cortex" of thick wall around an echogenic "sinus"
• These signs mean abnormal wall thickening, not a diagnosis. Causes include neoplasm, inflammation (Crohn disease, infection), intussusception, and ischemia

4Acute Appendicitis

• The appendix arises from the cecum, below the ileocecal valve. Its position varies (pelvic, retrocecal, subhepatic)
• Clinical: periumbilical pain that migrates to the right lower quadrant, fever, nausea, elevated WBC, rebound tenderness. Maximal tenderness classically at McBurney point, about one-third of the way from the right ASIS to the umbilicus
• Landmarks: find the cecum and terminal ileum, then look anterior to the psoas muscle and the external iliac artery and vein

Signs of perforation

• Loss of the echogenic submucosal layer (a break in the wall)
• Periappendiceal fluid collection or abscess, often complex
• An appendicolith outside the appendix lumen
• The appendix may decompress after rupture and become harder to see, while pain may briefly ease

5Hypertrophic Pyloric Stenosis

• Thickening of the pyloric muscle narrows and lengthens the pyloric channel and blocks gastric emptying
• Typical patient: an infant about 2–12 weeks old (most often 3–6 weeks), more often male
• Clinical: projectile, non-bilious vomiting after feeds, a hungry baby, and a palpable "olive" in the epigastrium/RUQ
• Technique: high-frequency linear probe. Place the infant right side down (right posterior oblique) and give a small feed so fluid fills the antrum and outlines the pylorus. Watch for fluid passing through the channel

• Transverse: a target / donut sign: thick hypoechoic muscle around echogenic mucosa
• Long axis: the cervix sign: the elongated, thickened pylorus resembles a uterine cervix. Redundant mucosa bulging into the antrum is the antral nipple sign

6Intussusception

• A segment of bowel (the intussusceptum) telescopes into the next segment (the intussuscipiens)
• Ileocolic is the most common type in children; it usually lies in the right abdomen, often subhepatic
• Typical age: about 6 months to 3 years. In children it is usually idiopathic; in adults (and older children) look for a lead point such as a tumor or Meckel diverticulum
• Clinical: intermittent colicky pain (drawing up the legs), vomiting, a palpable sausage-shaped mass, and "red currant jelly" stool, a late sign

• Treatment: image-guided air or hydrostatic (contrast or saline) enema reduction; surgery if reduction fails or with perforation
• Short, small small bowel–small bowel intussusceptions are often transient and resolve on their own

7Obstruction & Ileus

• Keyboard (piano-key) sign: fluid-filled, dilated jejunum outlining the valvulae conniventes like keys on a keyboard
• Collapsed bowel beyond the dilated loops suggests a mechanical obstruction
• Worrisome findings: free fluid between loops, a thickened wall, and absent peristalsis in a previously active obstruction can mean ischemia or strangulation

8Inflammation & Neoplasm

Crohn disease

• Chronic transmural inflammatory bowel disease with skip lesions; the terminal ileum is the most commonly involved segment
• Sonographic findings: a thickened, rigid, often hyperemic bowel wall (target/pseudokidney), narrowed lumen, and reduced peristalsis
• Creeping fat: echogenic, thickened mesenteric fat wrapping around the diseased loop
• Complications: strictures, fistulas, abscesses, and enlarged mesenteric lymph nodes
• Ulcerative colitis, by contrast, involves the mucosa of the colon continuously, starting at the rectum

Diverticulitis

• Inflammation of a colonic diverticulum (an outpouching of the wall), most often in the sigmoid colon, causing left lower quadrant pain in older adults
• Findings: segmental colon wall thickening, an inflamed diverticulum seen as a hypoechoic or echogenic outpouching (sometimes with a shadowing fecalith or gas), surrounding echogenic inflamed fat, and focal tenderness. Look for an abscess

GI tract neoplasm

• Usually a focal, irregular, asymmetric, hypoechoic wall thickening with loss of the layers: a target lesion or pseudokidney
• Long segments of very hypoechoic thickening suggest lymphoma; look for liver metastases and enlarged nodes

9Midgut Malrotation & Volvulus

• Malrotation: abnormal fetal rotation of the midgut leaves the bowel on a narrow mesenteric base that can twist (midgut volvulus), cutting off blood supply
• Clinical: a newborn or young infant with bilious (green) vomiting, a surgical emergency
• Normal relationship: the SMV lies to the right of the SMA, and the 3rd part of the duodenum crosses between the SMA and aorta
• Malrotation: reversal of the relationship, with the SMV to the left of or directly anterior to the SMA
• Volvulus: the whirlpool sign: on color Doppler, the SMV and mesentery wrap around the SMA (classically clockwise). Proximal duodenal dilation may also be seen

1The Peritoneum

• The peritoneum is a thin serous membrane lining the abdominopelvic cavity
• Parietal peritoneum lines the abdominal wall; visceral peritoneum covers the surface of the organs
• The potential space between the two layers is the peritoneal cavity. Normally it holds only a few mL of lubricating fluid, too little to see on ultrasound
• The cavity has two parts: the greater sac (most of the cavity) and the lesser sac (omental bursa) behind the stomach. They connect through the epiploic foramen (foramen of Winslow)
• Mesentery and omentum are double folds of peritoneum that carry vessels to the bowel and suspend organs. The greater omentum hangs like an apron from the stomach over the bowel

Intraperitoneal vs retroperitoneal

• Intraperitoneal organs are almost completely wrapped in visceral peritoneum: liver (except the bare area), gallbladder, spleen, stomach, the first part of the duodenum, jejunum and ileum, transverse and sigmoid colon, and the appendix
• Retroperitoneal organs lie behind the posterior parietal peritoneum, covered only on their anterior surface

2Peritoneal Spaces Where Fluid Collects

• Morison pouch (right posterior subhepatic space, hepatorenal recess): between the liver and right kidney. It is the most dependent space in the upper abdomen with the patient supine
• Subphrenic spaces (right and left): between the diaphragm and the liver or spleen. On the right, they are separated from the subhepatic space by the coronary ligament around the bare area
• Subhepatic space (anterior and posterior): below the liver; the posterior part is Morison pouch
• Paracolic gutters: channels lateral to the ascending and descending colon. The right gutter is larger and connects Morison pouch to the pelvis. The left is partly blocked above by the phrenicocolic ligament
• Lesser sac: between the stomach and pancreas. Fluid here classically comes from pancreatitis or a perforated posterior gastric ulcer
• Pelvis: the pouch of Douglas (rectouterine pouch) in women and the rectovesical pouch in men are the most dependent spaces in the whole peritoneal cavity

3Ascites, Abscess & Hematoma

Ascites

• Ascites = abnormal fluid in the peritoneal cavity. Small amounts first appear in Morison pouch and the pelvis; large amounts fill the gutters and surround the liver
• With large ascites, gas-filled bowel loops float centrally, tethered by the mesentery

Abscess and hematoma

• Abscess: a complex collection with thick, irregular walls, internal debris, fluid-debris levels, and septations. Gas inside appears as bright foci with dirty shadowing or ring-down. Clinically: fever and elevated WBC, often after surgery. Common sites: subphrenic, subhepatic, pelvic
• Hematoma: appearance changes with age. Very fresh blood can be anechoic; once it clots it becomes echogenic; over days to weeks it liquefies, becoming complex then more anechoic, often with septations. History: trauma, surgery, a procedure, or anticoagulation

4The FAST Exam

• FAST = Focused Assessment with Sonography in Trauma. A rapid bedside search for free fluid, presumed to be blood in the trauma patient
• It answers one question: is there free fluid? It is not a full organ survey

• eFAST (extended FAST) adds both anterior chest windows for pneumothorax (look for lung sliding) and the lung bases for hemothorax
• Absent lung sliding suggests pneumothorax; in M-mode, normal lung gives the "seashore" pattern and pneumothorax gives the "barcode" (stratosphere) pattern

5Retroperitoneal Compartments

• The retroperitoneum extends from the diaphragm to the pelvic brim, between the posterior parietal peritoneum and the transversalis fascia
• The renal fascia divides it into three compartments. The anterior layer is Gerota fascia; the posterior layer is often called Zuckerkandl fascia

• The aorta, IVC, and the para-aortic lymph nodes lie in the midline retroperitoneum, often described as a separate great vessel space
• The psoas and quadratus lumborum muscles form the posterior wall

6Retroperitoneal Fluid & Lymph Nodes

Fluid collections

• Urinoma: urine leaking from the collecting system, ureter, or bladder after trauma, surgery, or obstruction. Usually anechoic, near the kidney or ureter, and can be large
• Lymphocele: lymph collecting after surgery that disrupts lymphatics, classically after renal transplant or pelvic node dissection. Anechoic, often septated, usually appearing weeks to months after surgery. Near a transplant it can compress the ureter and cause hydronephrosis
• Hematoma: from trauma, anticoagulation, a procedure, or a leaking aortic aneurysm. Complex, evolving appearance (see section 3)

Lymph nodes

• Enlarged nodes are usually hypoechoic, especially in lymphoma, and can look almost anechoic but lack posterior enhancement
• Mantle sign: nodes draped around the aorta and IVC; bulky nodes can lift the aorta away from the spine
• Sandwich sign: mesenteric nodes on both sides of the SMA/SMV, with the vessels as the "filling"

7Fibrosis, Tumors & the Psoas

Retroperitoneal fibrosis

• A fibrous plaque around the aorta, IVC, and iliac vessels, usually centered around the lower lumbar spine and extending toward the iliacs
• Most cases are idiopathic (Ormond disease); others are linked to medications, malignancy, aneurysm, or prior radiation
• Sonographic look: a hypoechoic, smooth-margined mantle of tissue that encases the vessels
• It entraps the ureters, pulling them medially and causing bilateral hydronephrosis

Primary retroperitoneal tumors

• Tumors arising in the retroperitoneum, not from a retroperitoneal organ. Most are malignant
• Liposarcoma is the most common primary retroperitoneal malignancy. Its fat content often makes it echogenic, so it can blend with surrounding fat and be underestimated
• Leiomyosarcoma is next most common; it can arise from the IVC wall. Others include undifferentiated sarcomas and neurogenic tumors
• They often grow very large before causing symptoms and displace organs (for example, pushing a kidney anteriorly)

Psoas and iliopsoas

• Normal psoas: hypoechoic muscle with fine echogenic fibrous striations, running from the lumbar spine to join the iliacus as the iliopsoas
• Psoas hematoma: classically in anticoagulated patients or after femoral catheterization
• Psoas abscess: spread from the spine, kidney, or bowel (for example, Crohn disease or TB). Patients may hold the hip flexed
• Compare left to right: an enlarged, more heterogeneous psoas is the clue

8Guided Procedures: Before the Needle

• Biopsy: sampling of a mass or organ
  • FNA (fine-needle aspiration): thin needle, roughly 20–25 gauge. Yields cells for cytology. Lower bleeding risk
  • Core biopsy: larger needle, roughly 14–20 gauge, often spring-loaded. Yields a tissue core for histology, preserving architecture. Higher bleeding risk
• Paracentesis: drainage of ascites, diagnostic or therapeutic. A deep pocket, often in a lower quadrant lateral to the rectus muscle, avoiding bowel and the inferior epigastric vessels
• Thoracentesis: drainage of a pleural effusion. Patient usually sitting upright, leaning forward; the needle passes over the top of a rib to avoid the neurovascular bundle under each rib
• Drain placement: a catheter left in an abscess or collection for ongoing drainage

Pre-procedure checklist

• Labs: coagulation studies, chiefly PT/INR (and often PTT) and the platelet count. Typical thresholds for higher-risk biopsies are an INR of about 1.5 or less and platelets above about 50,000/µL; exact cutoffs vary by facility and procedure risk
• Medications: anticoagulants and antiplatelet drugs are reviewed and held as directed
• Informed consent: the physician explains risks, benefits, and alternatives and obtains it; the sonographer may act as a witness
• Time-out: just before the procedure, the whole team pauses to confirm the correct patient, procedure, and site/side
• Sterile technique: skin prep (such as chlorhexidine), sterile drapes, sterile probe cover and sterile gel, sterile gloves

9Needle Visualization & Aftercare

• Needle guide: a bracket attached to the transducer fixes the needle's angle; on-screen biopsy guidelines show the expected path. Freehand technique gives more flexibility but takes practice
• Needles are seen best when closer to perpendicular to the beam; steep angles reflect sound away. Beam steering, slight needle movement ("jiggle"), and echogenic-tip needles help
• A bright needle often shows reverberation (comet-tail) artifact behind it

After the procedure

• Rescan the site for a new hematoma or growing fluid collection, and document it
• Pneumothorax awareness: after thoracentesis or any upper abdominal or chest-wall pass near the lung, watch for shortness of breath or chest pain. Absent lung sliding on ultrasound, or a chest X-ray, can confirm
• Monitor vital signs, label specimens correctly, and record the procedure, needle size, number of passes, and any complications

1Before the Scan

• Introduce yourself, then confirm identity with two identifiers: full name and date of birth
• Confirm the reason for the exam and check that the order has an accurate clinical indication. A wrong or vague indication can get the exam denied by insurance
• Take a reproductive history:
  • LMP (first day of the last menstrual period)
  • Gravidity and parity
  • Miscarriages, abortions, and ectopic pregnancies
  • Current pain or bleeding, and any prior pelvic surgery (hysterectomy, C-section, oophorectomy)

2Transabdominal Prep: The Full Bladder

• Transabdominal (TA) pelvic scanning is done from the anterior abdomen and needs a full urinary bladder
• A typical prep: drink 32 oz of water, finished 1 hour before the exam, and don't void. Postmenopausal patients usually need only about 24 oz, since the uterus is smaller
• Prep amounts vary by facility, so always follow the site's protocol
• A reminder call the day before saves exams. A common mistake is drinking the water and then emptying the bladder

• Overfilled bladder? It can compress the uterus, push the ovaries out of view, and create so much posterior enhancement that deep structures wash out. Have the patient partially void, for example urinate for a count of about five seconds and stop, then rescan

3Transabdominal Technique

• Position: supine, muscles relaxed. Bending one knee can ease the discomfort of a full bladder
• Transducer: low-frequency curved array, about 3.5–5 MHz, for penetration
• Pressure: firmer than feels natural often improves the image a lot. Keep your arm close to your body to protect your shoulder (rotator cuff) over a career

A typical sequence

• Sagittal, midline: the uterus with and without measurements: length, height (AP), and endometrial thickness. Color Doppler over the endometrium can highlight pathology
• Sagittal sweep to the right and left of midline
• Transverse, inferior to superior: vagina and cervix → body (corpus) → fundus. Measure width at the widest point
• Ovaries last: use the internal iliac vessels as landmarks; the ovary usually lies just anterior/medial to them

4Transvaginal Technique

• Usually done right after the TA exam, from the inferior aspect of the body
• Bladder completely empty: even a little urine can push the anatomy out of the probe's short field of view
• Position: lithotomy (feet in stirrups), or hips raised on a wedge or pillow; undressed from the waist down under a sheet
• Consent is obtained because the exam is invasive. A chaperone is offered per facility policy and is standard when the sonographer is male
• Transducer: high-frequency endocavitary probe (roughly 5–10 MHz), with gel inside and outside a probe cover, inserted only a few inches into the vaginal canal
• Between patients: remove the cover and perform high-level disinfection, commonly with an automated hydrogen peroxide system that takes several minutes per cycle

• Not performed: in patients who have never been sexually active, or when the patient declines. Use TA or transperineal scanning instead
• Posterior cul-de-sac (pouch of Douglas): the space between the uterus and rectum, the most dependent spot in the pelvis. A small amount of free fluid there is normal, often after ovulation

5Image Orientation

• TA sagittal: anterior at the top, posterior at the bottom, superior (head) on screen left, inferior (feet) on screen right
• TV sagittal: the probe enters from below, so the image is the TA view rotated 90° counterclockwise: inferior at the top, superior at the bottom, anterior on screen left, posterior on screen right
• The TV "transverse" plane is technically a coronal plane; the patient's right is on screen left, as usual

6Obstetric Prep & Transperineal Scanning

• Before about 15 weeks: same prep as a TA pelvic exam (full bladder)
• After about 15 weeks: amniotic fluid becomes the acoustic window. Only a partly filled bladder (around 16 oz) is needed to help see the cervix and lower uterine segment
• After the first trimester, TA is the main approach. TV or transperineal views are added when the cervix or the lower edge of the placenta needs a closer look

Transperineal (translabial) scanning

• A curved transducer, covered with a probe cover or gel-filled glove, is placed against the perineum, between the labia
• Used mainly for the cervix and placental location when TV scanning isn't appropriate (for example, ruptured membranes or the patient declines)
• Key questions it answers: placenta previa and cervical insufficiency (incompetent cervix: painless, premature cervical shortening and dilation)

7Sonohysterography

• Also called saline infusion sonohysterography (SIS)
• A thin catheter is passed through the cervix into the uterine cavity, and a small volume of sterile saline (often up to about 20–30 mL) is infused to distend the endometrial cavity
• The physician (radiologist or OB/GYN) places the catheter; the sonographer runs the machine and scans transvaginally
• Timing: early in the cycle, after bleeding stops and before ovulation (to avoid disturbing a possible pregnancy). Not done in pregnancy or with active pelvic infection

• Finds: endometrial polyps, submucosal fibroids, endometrial hyperplasia, adhesions, and suspected endometrial cancer
• Infertility: with saline, air, or a contrast agent, it can also show whether the fallopian tubes are patent

8Emerging Tools: Contrast & 3D/4D

• Ultrasound contrast agents improve color and pulsed-wave Doppler of small uterine and ovarian vessels, which can help tell benign from malignant masses
• 3D = a volume of data; 4D = 3D in real time (motion)
• 3D/4D is best for external fetal surfaces: the face (e.g., cleft lip), digits and limbs, the umbilical cord, and neural tube defects of the spine
• In GYN, the 3D coronal view of the uterus helps show uterine shape anomalies and IUD position

9The Sonographer's Responsibilities

• Provide the right equipment for the exam
• Minimize discomfort and protect the patient's privacy and dignity
• Limit exposure: scan only as long as needed with the lowest output that gets the image (ALARA)
• Perform a thorough, systematic exam every time
• Follow the sonographer's code of ethics / professional conduct

Credentials & CME

• ARDMS credentials are earned by specialty: passing the SPI plus a specialty exam (e.g., OB/GYN, Abdomen) earns the RDMS in that specialty
• To keep credentials active, ARDMS currently requires 30 CME credits every 3 years
• CME is easier to earn than it sounds: online courses and simulation platforms, seminars and conferences, and vendor training on new equipment can all count when accredited

1Why Sonographers Care

• The endometrium changes thickness and appearance through the cycle, and you can see those changes on ultrasound
• A "normal" thickness depends on where the patient is in her cycle. A lining that would be normal on day 22 could be abnormal on day 4
• That's why you always ask for the first day of the last menstrual period (LMP) before a pelvic scan

2The Cycle at a Glance

• Starts at menarche (first period, usually around ages 10–14) and ends at menopause (usually ages 45–55), defined as 12 months with no period
• The average cycle is 28 days, counted from day 1 of bleeding. Normal adult cycles range roughly 21–35 days
• Two cycles run side by side: the ovarian cycle (what the follicles do) and the uterine/endometrial cycle (what the lining does)

3The Three Uterine Phases

Menstrual phase (days 1–5)

• Starts on day 1 of bleeding and lasts about 5 days (it varies)
• Estrogen and progesterone have dropped, so the functional layer of the endometrium breaks down and is shed as menses
• The uterus contracts rhythmically to expel the tissue. Those contractions cause menstrual cramps
• Flow is usually heaviest for the first 12–24 hours, then tapers off over the next several days
• Length varies: often shorter on birth control pills, and can be longer with uterine fibroids
• Sono: a thin, bright, pencil-line endometrium; a little blood may be seen in the cavity

Proliferative phase (days 6–14), the estrogen phase

• Begins when bleeding stops and ends at ovulation
• Estrogen from the growing follicles rebuilds the lining, so it steadily thickens
• Sono: the lining thickens around the central echogenic line. Near ovulation it shows the classic trilaminar ("three-line") pattern: bright outer lines, a darker functional layer, and a bright central line

Secretory phase (days 15–28), the luteal / progesterone phase

• Begins at ovulation and ends when the next period starts
• Progesterone (plus estrogen) from the corpus luteum makes the lining glandular and highly vascular to prepare for implantation
• No pregnancy? The corpus luteum fades, hormones fall, and menses begins again
• Sono: the thickest endometrium of the cycle, uniformly echogenic, often with posterior acoustic enhancement

4Endometrial Thickness on Ultrasound

• How to measure: in a sagittal (long-axis) view of the uterus, measure the full double-layer thickness at the thickest point, anterior to posterior, from echogenic edge to echogenic edge
• Don't include fluid in the cavity (measure each layer and add them) or the thin dark halo of inner myometrium

5Hormonal Control

• The hypothalamus also controls body temperature, hunger, thirst, and sleep cycles
• The pea-sized anterior pituitary also makes prolactin (milk production). Oxytocin (contractions, milk let-down) comes from the posterior pituitary
• Where they are: the hypothalamus sits just below the thalamus. The pituitary hangs beneath it, protected in a bony pocket of the skull base called the sella turcica ("Turkish saddle"). Its anterior lobe is the larger of the two
• The pituitary steers most of the body's other endocrine glands, which is why it is often called the "master gland"

The chain of events

1. Hypothalamus releases GnRH
2. Anterior pituitary releases FSH
3. FSH recruits a group of follicles (often 5–7 visible); they grow and make estrogen
4. Rising estrogen triggers the LH surge
5. The LH surge makes the dominant graafian follicle (about 1.8–2.5 cm) rupture and release the egg: ovulation
6. The ruptured follicle becomes the corpus luteum, which makes progesterone
7. No pregnancy → the corpus luteum degenerates (into a small scar, the corpus albicans), hormones drop, and menses starts

6Ovulation on Ultrasound

• Each cycle FSH recruits a small group of follicles, often 5–7. One becomes dominant (the graafian follicle); the rest stop growing and degenerate, a process called atresia
• At ovulation the graafian follicle ruptures through the ovary's surface and its tough outer capsule, the tunica albuginea. The egg is swept up by the fimbriae into the funnel-shaped open end of the tube, the infundibulum
• The graafian follicle usually ruptures at about 1.8–2.5 cm (average about 2.0 cm)
• Ovaries are smooth early in life and become more irregular and scarred over the reproductive years from repeated ovulation
• The follicle releases a little fluid or blood, so a small amount of free fluid in the posterior cul-de-sac around mid-cycle is normal
• Mittelschmerz ("middle pain"): mild one-sided pelvic pain at ovulation from that fluid irritating the pelvis. It lasts from a few hours to about a day

7Abnormal Bleeding Terms

These terms often show up as the indication on the order.

• Primary amenorrhea: has never had a period (evaluated by about age 15). Causes include anatomic anomalies or an obstruction
• Secondary amenorrhea: periods started, then stopped. Pregnancy is the most common cause; others include low body weight, poor nutrition, and intense athletic training

8Birth Control & Hormone Replacement

Hormonal contraceptives

• Most hormonal birth control suppresses FSH and LH, which prevents ovulation
• Result: more regular, predictable cycles with shorter, lighter periods and usually a thin endometrium
• Non-hormonal methods like the copper IUD don't stop ovulation. They make the uterus hostile to sperm and implantation

Hormone replacement therapy (HRT)

• Replaces hormones the ovaries no longer make after menopause: estrogen, often with a progestin (synthetic progesterone)
• Treats hot flashes, mood and sleep changes, and vaginal dryness
• Use has dropped because long-term HRT is linked to a higher risk of some cancers, notably breast cancer, and endometrial cancer when estrogen is given without a progestin

1Why Sonographers Care

• Congenital anomalies of the reproductive tract are uncommon, and most patients have no symptoms
• They are easy to miss or misread. A second uterine horn can look like a fibroid, an adnexal mass, or even a twin pregnancy
• The reproductive and urinary tracts develop side by side in the embryo, so reproductive anomalies often come with kidney anomalies (renal agenesis is the classic pairing)

2How the Uterus Forms

• Two Müllerian (paramesonephric) ducts grow toward the midline and fuse to form the uterus, cervix, and upper vagina. Their unfused upper ends become the fallopian tubes
• Right after fusion there is a wall (septum) down the middle. It is normally reabsorbed, finishing around 20 weeks of development, leaving one cavity
• The ovaries develop separately, so they are usually normal even when the uterus is not
• In females the Wolffian (mesonephric) ducts mostly disappear. Leftover bits can form cysts later (Gartner duct and paraovarian cysts, section 8)

3Outflow Obstruction & Vaginal Anomalies

• Usually shows up at puberty, when menstrual blood has nowhere to go
• Symptoms: cyclic pelvic pain, primary amenorrhea (no period despite normal development), dysmenorrhea, dyspareunia (painful intercourse)
• Causes: imperforate hymen (most common), a transverse vaginal septum, or cervical atresia

• Sono: a distended vagina and/or uterine cavity filled with fluid containing low- to mid-level echoes (old blood). Whatever is distended sits above the blockage
• Vaginal agenesis = absent vagina. Vaginal atresia = vagina failed to develop normally
• MRKH (Mayer-Rokitansky-Küster-Hauser) syndrome: absent or tiny uterus plus absent upper vagina, with normal ovaries, so puberty otherwise looks normal. Presents as primary amenorrhea

4Uterine Anomalies

• The most common duplication anomalies are septate, bicornuate, and didelphys. They may or may not come with vaginal anomalies